Una enfermedad lejana: la información sobre poliomielitis y síndrome post-polio en la prensa hispanolusa, 1995-2009

Se explora el cambio en la percepción social de la polio en la Península Ibérica a través del análisis de contenidos, entre 1995 y 2009, de dos periódicos de gran tirada. La desaparición en la agenda periodística de la polio y de las personas que viven con sus secuelas influyó en el olvido de la misma en la agenda pública. La poliomielitis se vinculó a la pobreza y la ignorancia en países lejanos, susceptibles de acciones de cooperación, siendo objeto de atención solo cuando es percibida como amenaza para Occidente, vinculada a crisis sanitarias o en un sentido metafórico. Así, el síndrome post-polio fue invisibilizado en el caso portugués y débilmente representado en España por el movimiento asociativo

Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture

Bone mineral density (BMD) is the most widely used predictor of fracture risk. We performed the largest meta-analysis to date on lumbar spine and femoral neck BMD, including 17 genome-wide association studies and 32,961 individuals of European and east Asian ancestry. We tested the top BMD-associated markers for replication in 50,933 independent subjects and for association with risk of low-trauma fracture in 31,016 individuals with a history of fracture (cases) and 102,444 controls. We identified 56 loci (32 new) associated with BMD at genome-wide significance (P < 5 x 10<sup>-8</sup>)). Several of these factors cluster within the RANK-RANKL-OPG, mesenchymal stem cell differentiation, endochondral ossification and Wnt signaling pathways. However, we also discovered loci that were localized to genes not known to have a role in bone biology. Fourteen BMD-associated loci were also associated with fracture risk (P < 5 x 10<sup>-4</sup>), Bonferroni corrected), of which six reached P < 5 x 10<sup>-8</sup>, including at 18p11.21 (FAM210A), 7q21.3 (SLC25A13), 11q13.2 (LRP5), 4q22.1 (MEPE), 2p16.2 (SPTBN1) and 10q21.1 (DKK1). These findings shed light on the genetic architecture and pathophysiological mechanisms underlying BMD variation and fracture susceptibility