Far Ultraviolet Spectra of B Stars near the Ecliptic

Spectra of B stars in the wavelength range of 911-1100 A have been obtained with the EURD spectrograph onboard the Spanish satellite MINISAT-01 with ~5 A spectral resolution. IUE spectra of the same stars have been used to normalize Kurucz models to the distance, reddening and spectral type of the corresponding star. The comparison of 8 main-sequence stars studied in detail (alpha Vir, epsilon Tau, lambda Tau, tau Tau, alpha Leo, zeta Lib, theta Oph, and sigma Sgr) shows agreement with Kurucz models, but observed fluxes are 10-40% higher than the models in most cases. The difference in flux between observations and models is higher in the wavelength range between Lyman alpha and Lyman beta. We suggest that Kurucz models underestimate the FUV flux of main-sequence B stars between these two Lyman lines. Computation of flux distributions of line-blanketed model atmospheres including non-LTE effects suggests that this flux underestimate could be due to departures from LTE, although other causes cannot be ruled out. We found the common assumption of solar metallicity for young disk stars should be made with care, since small deviations can have a significant impact on FUV model fluxes. Two peculiar stars (rho Leo and epsilon Aqr), and two emission line stars (epsilon Cap and pi Aqr) were also studied. Of these, only epsilon Aqr has a flux in agreement with the models. The rest have strong variability in the IUE range and/or uncertain reddening, which makes the comparison with models difficult.Comment: 25 pages, 6 figures, to be published in The Astrophysical Journa

Progressive Shifts in the Gut Microbiome Reflect Prediabetes and Diabetes Development in a Treatment-Naive Mexican Cohort.

Type 2 diabetes (T2D) is a global epidemic that affects more than 8% of the world\u27s population and is a leading cause of death in Mexico. Diet and lifestyle are known to contribute to the onset of T2D. However, the role of the gut microbiome in T2D progression remains uncertain. Associations between microbiome composition and diabetes are confounded by medication use, diet, and obesity. Here we present data on a treatment-naive cohort of 405 Mexican individuals across varying stages of T2D severity. Associations between gut bacteria and more than 200 clinical variables revealed a defined set of bacterial genera that were consistent biomarkers of T2D prevalence and risk. Specifically, gradual increases in blood glucose levels, beta cell dysfunction, and the accumulation of measured T2D risk factors were correlated with the relative abundances of four bacterial genera. In a cohort of 25 individuals, T2D treatment-predominantly metformin-reliably returned the microbiome to the normoglycemic community state. Deep clinical characterization allowed us to broadly control for confounding variables, indicating that these microbiome patterns were independent of common T2D comorbidities, like obesity or cardiovascular disease. Our work provides the first solid evidence for a direct link between the gut microbiome and T2D in a critically high-risk population. In particular, we show that increased T2D risk is reflected in gradual changes in the gut microbiome. Whether or not these T2D-associated changes in the gut contribute to the etiology of T2D or its comorbidities remains to be seen

Lack of replication of interactions between polymorphisms in rheumatoid arthritis susceptibility: case-control study

Introduction: Approximately 100 loci have been definitively associated with rheumatoid arthritis (RA) susceptibility. However, they explain only a fraction of RA heritability. Interactions between polymorphisms could explain part of the remaining heritability. Multiple interactions have been reported, but only the shared epitope (SE) × protein tyrosine phosphatase nonreceptor type 22 (PTPN22) interaction has been replicated convincingly. Two recent studies deserve attention because of their quality, including their replication in a second sample collection. In one of them, researchers identified interactions between PTPN22 and seven single-nucleotide polymorphisms (SNPs). The other showed interactions between the SE and the null genotype of glutathione S-transferase Mu 1 (GSTM1) in the anti-cyclic citrullinated peptide-positive (anti-CCP+) patients. In the present study, we aimed to replicate association with RA susceptibility of interactions described in these two high-quality studies. Methods: A total of 1,744 patients with RA and 1,650 healthy controls of Spanish ancestry were studied. Polymorphisms were genotyped by single-base extension. SE genotypes of 736 patients were available from previous studies. Interaction analysis was done using multiple methods, including those originally reported and the most powerful methods described. Results: Genotypes of one of the SNPs (rs4695888) failed quality control tests. The call rate for the other eight polymorphisms was 99.9%. The frequencies of the polymorphisms were similar in RA patients and controls, except for PTPN22 SNP. None of the interactions between PTPN22 SNPs and the six SNPs that met quality control tests was replicated as a significant interaction term the originally reported finding or with any of the other methods. Nor was the interaction between GSTM1 and the SE replicated as a departure from additivity in anti-CCP+ patients or with any of the other methods. Conclusions: None of the interactions tested were replicated in spite of sufficient power and assessment with different assays. These negative results indicate that whether interactions are significant contributors to RA susceptibility remains unknown and that strict standards need to be applied to claim that an interaction exists

Pluripotency factors regulate the onset of Hox cluster activation in the early embryo

Pluripotent cells are a transient population of the mammalian embryo dependent on transcription factors, such as OCT4 and NANOG, which maintain pluripotency while suppressing lineage specification. However, these factors are also expressed during early phases of differentiation, and their role in the transition from pluripotency to lineage specification is largely unknown. We found that pluripotency factors play a dual role in regulating key lineage specifiers, initially repressing their expression and later being required for their proper activation. We show that Oct4 is necessary for activation of HoxB genes during differentiation of embryonic stem cells and in the embryo. In addition, we show that the HoxB cluster is coordinately regulated by OCT4 binding sites located at the 3′ end of the cluster. Our results show that core pluripotency factors are not limited to maintaining the precommitted epiblast but are also necessary for the proper deployment of subsequent developmental programs

Twilight Mesospheric Clouds in Jezero as Observed by MEDA Radiation and Dust Sensor (RDS)

The Mars Environmental Dynamics Analyzer instrument, on board NASA's Mars 2020 Perseverance rover, includes a number of sensors to characterize the Martian atmosphere. One of these sensors is the Radiation and Dust Sensor (RDS) that measures the solar irradiance at different wavelengths and geometries. We analyzed the RDS observations made during twilight for the period between sol 71 and 492 of the mission (Ls 39°–262°, Mars Year 36) to characterize the clouds over the Perseverance rover site. Using the ratio between the irradiance at zenith at 450 and 750 nm, we inferred that the main constituent of the detected high-altitude aerosol layers was ice from Ls = 39°–150° (cloudy period), and dust from Ls 150°–262°. A total of 161 twilights were analyzed in the cloudy period using a radiative transfer code and we found: (a) signatures of clouds/hazes in the signals in 58% of the twilights; (b) most of the clouds had altitudes between 40 and 50 km, suggesting water ice composition, and had particle sizes between 0.6 and 2 µm; (c) the cloud activity at sunrise is slightly higher that at sunset, likely due to the differences in temperature; (d) the time period with more cloud detections and with the greatest cloud opacities is during Ls 120°–150°; and (e) a notable decrease in the cloud activity around aphelion, along with lower cloud altitudes and opacities. This decrease in cloud activity indicates lower concentrations of water vapor or cloud condensation nuclei (dust) around this period in the Martian mesosphere.This work has been funded by the Spanish Ministry of Economy and Competitiveness, through the projects no. ESP2014-54256-C4-1-R (also ESP2014-54256-C4-2-R, ESP2014-54256-C4-3-R, and ESP2014-54256-C4-4-R), Spanish Ministry of Science, Innovation and Universities, projects no. ESP2016-79612-C3-1-R (also ESP2016-79612-C3-2-R and ESP2016-79612-C3-3-R), Spanish Ministry of Science and Innovation/State Agency of Research (10.13039/501100011033), projects no. PID2021-126719OB-C41, ESP2016-80320-C2-1-R, RTI2018-098728-B-C31 (also RTI2018-098728-B-C32 and RTI2018-098728-B-C33), RTI2018-099825-B-C31. RH and ASL were supported by the Spanish project PID2019-109467GB-I00 funded by MCIN/AEI/10.13039/50110001103 and by Grupos Gobierno Vasco IT1742-22. The US co-authors performed their work under sponsorship from NASA’s Mars 2020 project, from the Game Changing Development programme within the Space Technology Mission Directorate and from the Human Exploration and Operations Directorate. Part of this research was carried out at the Jet Propulsion Laboratory, California Institute of Technology, under a contract with the National Aeronautics and Space Administration (80NM0018D0004). G.M. acknowledges JPL funding from USRA Contract Number 1638782. ML is supported by contract 15-712 from Arizona State University and 1607215 from Caltech-JPL. A. V-R. is supported by the Comunidad de Madrid Project S2018/NMT-4291 (TEC2SPACE-CM)

Analysis of TNFAIP3, a feedback inhibitor of nuclear factor-κB and the neighbor intergenic 6q23 region in rheumatoid arthritis susceptibility

Introduction Genome-wide association studies of rheumatoid arthritis (RA) have identified an association of the disease with a 6q23 region devoid of genes. TNFAIP3, an RA candidate gene, flanks this region, and polymorphisms in both the TNFAIP3 gene and the intergenic region are associated with systemic lupus erythematosus. We hypothesized that there is a similar association with RA, including polymorphisms in TNFAIP3 and the intergenic region. Methods To test this hypothesis, we selected tag-single nucleotide polymorphisms (SNPs) in both loci. They were analyzed in 1,651 patients with RA and 1,619 control individuals of Spanish ancestry. Results Weak evidence of association was found both in the 6q23 intergenic region and in the TNFAIP3 locus. The rs582757 SNP and a common haplotype in the TNFAIP3 locus exhibited association with RA. In the intergenic region, two SNPs were associated, namely rs609438 and rs13207033. The latter was only associated in patients with anti-citrullinated peptide antibodies. Overall, statistical association was best explained by the interdependent contribution of SNPs from the two loci TNFAIP3 and the 6q23 intergenic region. Conclusions Our data are consistent with the hypothesis that several RA genetic factors exist in the 6q23 region, including polymorphisms in the TNFAIP3 gene, like that previously described for systemic lupus erythematosus

Decay of excited nuclei produced in 78,82Kr+40Ca reactions at 5.5 MeV/nucleon

Decay modes of excited nuclei are investigated in 78,82Kr+40Ca reactions at 5.5 MeV/nucleon. Charged products were measured by means of the 4π INDRA array. Kinetic-energy spectra and angular distributions of fragments with atomic number 3 Z 28 indicate a high degree of relaxation and are compatible with a fissionlike phenomenon. Persistence of structure effects is evidenced from elemental cross sections (σZ) as well as a strong odd-even staggering (o-e-s) of the light-fragment yields. The magnitude of the staggering does not significantly depend on the neutron content of the emitting system. Fragment-particle coincidences suggest that the light partners in very asymmetric fission are emitted either cold or at excitation energies below the particle emission thresholds. The evaporation residue cross section of the 78Kr+40Ca reaction is slightly higher than the one measured in the 82Kr+40Ca reaction. The fissionlike component is larger by ∼25% for the reaction having the lowest neutron-to-proton ratio. These experimental features are confronted to the predictions of theoretical models. The Hauser-Feshbach approach including the emission of fragments up to Z = 14 in their ground states as well as excited states does not account for the main features of σZ. For both reactions, the transition-state formalism reasonably reproduces the Z distribution of the fragments with charge 12 Z 28. However, this model strongly overestimates the light-fragment cross sections and does not explain the o-e-s of the yields for 6 Z 10. The shape of the whole Z distribution and the o-e-s of the light-fragment yields are satisfactorily reproduced within the dinuclear system framework which treats the competition among evaporation, fusion-fission, and quasifission processes. The model suggests that heavy fragments come mainly from quasifission while light fragments are predominantly populated by fusion. An underestimation of the cross sections for 16 Z 22 could signal a mechanism in addition to the capture process

Measurement of the Lifetime Difference Between B_s Mass Eigenstates

We present measurements of the lifetimes and polarization amplitudes for B_s --> J/psi phi and B_d --> J/psi K*0 decays. Lifetimes of the heavy (H) and light (L) mass eigenstates in the B_s system are separately measured for the first time by determining the relative contributions of amplitudes with definite CP as a function of the decay time. Using 203 +/- 15 B_s decays, we obtain tau_L = (1.05 +{0.16}/-{0.13} +/- 0.02) ps and tau_H = (2.07 +{0.58}/-{0.46} +/- 0.03) ps. Expressed in terms of the difference DeltaGamma_s and average Gamma_s, of the decay rates of the two eigenstates, the results are DeltaGamma_s/Gamma_s = (65 +{25}/-{33} +/- 1)%, and DeltaGamma_s = (0.47 +{0.19}/-{0.24} +/- 0.01) inverse ps.Comment: 8 pages, 3 figures, 2 tables; as published in Physical Review Letters on 16 March 2005; revisions are for length and typesetting only, no changes in results or conclusion

Lack of validation of genetic variants associated with anti-tumor necrosis factor therapy response in rheumatoid arthritis: a genome-wide association study replication and meta-analysis

Introduction: In this study, our aim was to elucidate the role of four polymorphisms identified in a prior large genome-wide association study (GWAS) in which the investigators analyzed the responses of patients with rheumatoid arthritis (RA) to treatment with tumor necrosis factor inhibitors (TNFi). The authors of that study reported that the four genetic variants were significantly associated. However, none of the associations reached GWAS significance, and two subsequent studies failed to replicate these associations. Methods: The four polymorphisms (rs12081765, rs1532269, rs17301249 and rs7305646) were genotyped in a total of 634 TNFi-treated RA patients of Spanish Caucasian origin. Four outcomes were evaluated: changes in the Disease Activity Score in 28 joints (DAS28) after 6 and 12 months of treatment and classification according to the European League Against Rheumatism (EULAR) response criteria at the same time points. Association with DAS28 changes was assessed by linear regression using an additive genetic model. Contingency tables of genotype and allele frequencies between EULAR responder and nonresponder patients were compared. In addition, we combined our data with those of previously reported studies in a meta-analysis including 2,998 RA patients. Results: None of the four genetic variants showed an association with response to TNFi in any of the four outcomes analyzed in our Spanish patients. In addition, only rs1532269 yielded a suggestive association (P = 0.0033) with the response to TNFi when available data from previous studies were combined in the meta-analysis. Conclusion: Our data suggest that the rs12081765, rs1532269, rs17301249 and rs7305646 genetic variants do not have a role as genetic predictors of TNFi treatment outcomes