7 research outputs found

    Crustal distribution in the central Gulf of Mexico from an integrated geophysical analysis

    Get PDF
    This study addresses the question of the crustal composition in the central part of the northern Gulf of Mexico (GOM) – the region of the major disagreement between published tectonic models. The location of the Ocean-Continental Boundary (OCB) for different tectonic models varies within 140 km (87 mi) in the study area. I have developed a 2D model integrating the seismic reflection and refraction data with potential fields (gravity and magnetics) along the profile through the debated region. Two alternative OCB locations were tested. The preferred model suggests the OCB position near the Sigsbee Escarpment, which is in agreement with the result of Eddy, 2014 and with the findings of the LithoSPAN experiment (Makris et al, 2015). However, the model with an alternative OCB location (further to the north of the Sigsbee Escarpment) may also satisfy the observed gravity and magnetic fields, although the crust in the oceanic domain is thicker than normal. Since the potential fields do not offer the unique answer, the other geophysical data should be examined, such as the Vp/Vs ratio. This parameter was analyzed for the LithoSPAN (Makris et al., 2015) and allowed distinguishing between continental and oceanic domains; it was also examined for GUMBO 3 and 4 (Duncan, 2013). However, the values of Vs derived during retraction experiment for GUMBO 2 are not publically available at this time

    Pathogenicity and Impact of HLA Class I Alleles in Aplastic Anemia Patients of Different Ethnicities

    Get PDF
    Acquired aplastic anemia (AA) is caused by autoreactive T cell-mediated destruction of early hematopoietic cells. Somatic loss of human leukocyte antigen (HLA) class I alleles was identified as a mechanism of immune escape in surviving hematopoietic cells of some patients with AA. However, pathogenicity, structural characteristics, and clinical impact of specific HLA alleles in AA remain poorly understood. Here, we evaluated somatic HLA loss in 505 patients with AA from 2 multi-institutional cohorts. Using a combination of HLA mutation frequencies, peptide-binding structures, and association with AA in an independent cohort of 6,323 patients from the National Marrow Donor Program, we identified 19 AA risk alleles and 12 non-risk alleles and established a potentially novel AA HLA pathogenicity stratification. Our results define pathogenicity for the majority of common HLA-A/B alleles across diverse populations. Our study demonstrates that HLA alleles confer different risks of developing AA, but once AA develops, specific alleles are not associated with response to immunosuppression or transplant outcomes. However, higher pathogenicity alleles, particularly HLA-B*14:02, are associated with higher rates of clonal evolution in adult patients with AA. Our study provides insights into the immune pathogenesis of AA, opening the door to future autoantigen identification and improved understanding of clonal evolution in AA
    corecore