12 research outputs found

    Constraining the evolution of cataclysmic variables via the masses and accretion rates of their underlying white dwarfs

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    We report on the masses (MWD), effective temperatures (⁠Teff⁠) and secular mean accretion rates (⁠⟨M˙⟩⁠) of 43 cataclysmic variable (CV) white dwarfs, 42 of which were obtained from the combined analysis of their Hubble Space Telescope ultraviolet data with the parallaxes provided by the Early Third Data Release of the Gaia space mission, and one from the white dwarf gravitational redshift. Our results double the number of CV white dwarfs with an accurate mass measurement, bringing the total census to 89 systems. From the study of the mass distribution, we derive ⟨MWD⟩=0.81+0.16/−0.20M⊙⁠, in perfect agreement with previous results, and find no evidence of any evolution of the mass with orbital period. Moreover, we identify five systems with MWD < 0.5M⊙, which are most likely representative of helium-core white dwarfs, showing that these CVs are present in the overall population. We reveal the presence of an anti-correlation between the average accretion rates and the white dwarf masses for the systems below the 2 − 3 h period gap. Since ⟨M˙⟩ reflects the rate of system angular momentum loss, this correlation suggests the presence of an additional mechanism of angular momentum loss that is more efficient at low white dwarf masses. This is the fundamental concept of the recently proposed empirical prescription of consequential angular momentum loss (eCAML) and our results provide observational support for it, although we also highlight how its current recipe needs to be refined to better reproduce the observed scatter in Teff and ⟨M˙⟩⁠, and the presence of helium-core white dwarfs

    Combined immunotherapy and antiangiogenic therapy of cancer with microencapsulated cells

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    http://www.liebertonline.comReproduced by generous permission of the publisher.An alternative form of gene therapy involves immunoisolation of a nonautologous cell line engineered to secrete a therapeutic product. Encapsulation of these cells in a biocompatible polymer serves to protect these allogeneic cells from host-versus-graft rejection while recombinant products and nutrients are able to pass by diffusion. This strategy was applied to the treatment of cancer with some success by delivering either interleukin 2 or angiostatin. However, as cancer is a complex, multifactorial disease, a multipronged approach is now being developed to attack tumorigenesis via multiple pathways in order to improve treatment efficacy. A combination of immunotherapy with angiostatic therapy was investigated by treating B16-F0/neu melanoma- bearing mice with intraperitoneally implanted, microencapsulated mouse myoblasts (C2C12) genetically modified to deliver angiostatin and an interleukin 2 fusion protein (sFvIL-2). The combination treatment resulted in improved survival, delayed tumor growth, and increased histological indices of antitumor activity (apoptosis and necrosis). In addition to improved efficacy, the combination treatment also ameliorated some of the undesirable side effects from the individual treatments that have led to the previous failure of the single treatments, for example, inflammatory response to IL-2 or vascular mimicry due to angiostatin. In conclusion, the combination of immuno- and antiangiogenic therapies delivered by immunoisolated cells was superior to individual treatments for antitumorigenesis activity, not only because of their known mechanisms of action but also because of unexpected protection against the adverse side effects of the single treatments. Thus, the concept of a "cocktail" strategy, with microencapsulation delivering multiple antitumor recombinant molecules to improve efficacy, is validated

    Restoring montane cloud forest: Establishment of three fagaceae species in the old fields of central Veracruz, Mexico

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    Objective To identify susceptibility loci for rheumatoid arthritis (RA) in Latin American individuals with admixed European and Amerindian genetic ancestry. Methods Genotyping was performed in 1,475 patients with RA and 1,213 control subjects, using a customized BeadArray containing 196,524 markers covering loci previously associated with various autoimmune diseases. Principal components analysis (EigenSoft package) and Structure software were used to identify outliers and define the population substructure. REAP software was used to define cryptic relatedness and duplicates, and genetic association analyses were conducted using Plink statistical software. Results A strong genetic association between RA and the major histocompatibility complex region was observed, localized within BTNL2/DRA-DQB1- DQA2 (P = 7.6 10 -10), with 3 independent effects. We identified an association in the PLCH2-HES5-TNFRSF14-MMEL1 region of chromosome 1 (P = 9.77 10 -6), which was previously reported in Europeans, Asians, and Native Canadians. We identified one novel putative association in ENOX1 on chromosome 13 (P = 3.24 10-7). Previously reported associations were observed in the current study, including PTPN22, SPRED2, STAT4, IRF5, CCL21, and IL2RA, although the significance was relatively moderate. Adjustment for Amerindian ancestry improved the association of a novel locus in chromosome 12 at C12orf30 (NAA25) (P = 3.9 10-6). Associations with the HLA region, SPRED2, and PTPN22 improved in individuals positive for anti-cyclic citrullinated peptide antibodies. Conclusion Our data define, for the first time, the contribution of Amerindian ancestry to the genetic architecture of RA in an admixed Latin American population by confirming the role of the HLA region and supporting the association with a locus in chromosome 1. In addition, we provide data for novel putative loci in chromosomes 12 and 13. Copyright " 2013 by the American College of Rheumatology.",,,,,,"10.1002/art.37923",,,"http://hdl.handle.net/20.500.12104/44274","http://www.scopus.com/inward/record.url?eid=2-s2.0-84878560466&partnerID=40&md5=05744386464e335942f72691517049a5",,,,,,"6",,"Arthritis and Rheumatism",,"145

    Rheumatoid arthritis in latin americans enriched for amerindian ancestry is associated with loci in chromosomes 1, 12, and 13, and the HLA Class II region

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    Objective To identify susceptibility loci for rheumatoid arthritis (RA) in Latin American individuals with admixed European and Amerindian genetic ancestry. Methods Genotyping was performed in 1,475 patients with RA and 1,213 control subjects, using a customized BeadArray containing 196,524 markers covering loci previously associated with various autoimmune diseases. Principal components analysis (EigenSoft package) and Structure software were used to identify outliers and define the population substructure. REAP software was used to define cryptic relatedness and duplicates, and genetic association analyses were conducted using Plink statistical software. Results A strong genetic association between RA and the major histocompatibility complex region was observed, localized within BTNL2/DRA-DQB1- DQA2 (P = 7.6 × 10 -10), with 3 independent effects. We identified an association in the PLCH2-HES5-TNFRSF14-MMEL1 region of chromosome 1 (P = 9.77 × 10 -6), which was previously reported in Europeans, Asians, and Native Canadians. We identified one novel putative association in ENOX1 on chromosome 13 (P = 3.24 × 10-7). Previously reported associations were observed in the current study, including PTPN22, SPRED2, STAT4, IRF5, CCL21, and IL2RA, although the significance was relatively moderate. Adjustment for Amerindian ancestry improved the association of a novel locus in chromosome 12 at C12orf30 (NAA25) (P = 3.9 × 10-6). Associations with the HLA region, SPRED2, and PTPN22 improved in individuals positive for anti-cyclic citrullinated peptide antibodies. Conclusion Our data define, for the first time, the contribution of Amerindian ancestry to the genetic architecture of RA in an admixed Latin American population by confirming the role of the HLA region and supporting the association with a locus in chromosome 1. In addition, we provide data for novel putative loci in chromosomes 12 and 13. Copyright © 2013 by the American College of Rheumatology
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