Bolsa familia y la asistencia social en Brasil: de la lucha política a la mercantilización local

El propósito de este artículo es tanto teórico como metodológico: busca contribuir a la reflexión de la sociología acerca de los usos de las políticas sociales, mostrando que el estudio de una determinada "política" como Bolsa Familia requiere un dispositivo de investigación multi-escalar que permita captar los diversos conflictos que atraviesan su concretización, desde su emergencia hasta su despliegue en el territorio. En este sentido, a modo de ejercicio, se interroga la trayectoria de implementación del programa Bolsa Familia en dos momentos distintos en torno a su tecnología política "por arriba" y "por abajo": como dispositivo de gobierno (Foucault, 1976), emblemático durante el período de "Lula", y como dispositivo de gestión del territorio y de las poblaciones a través de la externalización o tercerización asistencial. En uno y otro momento, lo social adquiere valor de "mercadería política" a distintos niveles. Mostraremos cómo se produce en ellos el despliegue de la política de asistencia social: a nivel de Estado y lo público, y a nivel del territorio y la acción privada y no gubernamental. A nivel de su concretización, mostraremos, a partir de un caso de estudio en São Paulo, la importancia de seguir la cadena de producción de la política. Destacaremos, así, algunos elementos centrales de lo que podría ser llamado un modelo "PSDB", vigente en esa ciudad, como veremos al final

N-terminal domain of human Hsp90 triggers binding to the co-chaperone p23

The molecular chaperone Hsp90 is a protein folding machine that is conserved from bacteria to man. Human, cytosolic Hsp90 is dedicated to folding of chiefly signal transduction components. The chaperoning mechanism of Hsp90 is controlled by ATP and various cochaperones, but is poorly understood and controversial. Here, we characterized the Apo and ATP states of the 170-kDa human Hsp90 full-length protein by NMR spectroscopy in solution, and we elucidated the mechanism of the inhibition of its ATPase by its cochaperone p23. We assigned isoleucine side chains of Hsp90 via specific isotope labeling of their δ-methyl groups, which allowed the NMR analysis of the full-length protein. We found that ATP caused exclusively local changes in Hsp90’s N-terminal nucleotide-binding domain. Native mass spectrometry showed that Hsp90 and p23 form a 2∶2 complex via a positively cooperative mechanism. Despite this stoichiometry, NMR data indicated that the complex was not fully symmetric. The p23-dependent NMR shifts mapped to both the lid and the adenine end of Hsp90’s ATP binding pocket, but also to large parts of the middle domain. Shifts distant from the p23 binding site reflect p23-induced conformational changes in Hsp90. Together, we conclude that it is Hsp90’s nucleotide-binding domain that triggers the formation of the Hsp902p232 complex. We anticipate that our NMR approach has significant impact on future studies of full-length Hsp90 with cofactors and substrates, but also for the development of Hsp90 inhibiting anticancer drugs

Spatial distribution of cerebral microbleeds and FLAIR hyperintensities on follow-up MRI after radiotherapy for lower grade glioma

Background and purpose: Cerebral microbleeds (CMBs) and fluid-attenuated-inversion recovery (FLAIR) hyperintensities on brain MRI scans after radiotherapy (RT) are considered markers for microvascular damage and related cognitive changes. However, the spatial distribution using existing scoring systems as well as colocation of these imaging biomarkers remain unclear, hampering clinical interpretation. This study aims to elucidate the distribution and colocation of these markers in patients with lower grade glioma (LGG). Materials and methods: CMBs were spatially classified on retrospective 1.5 T susceptibility weighted MRI scans according to the existing Microbleed Anatomical Rating Scale (MARS) and were additionally scored for being located in hippocampus, amygdala, cortex, white matter (WM), grey matter (GM), WM/GM junction and for their spatial relation to FLAIR hyperintensities. Scoring was performed for whole, ipsilateral and contralateral cerebrum (with respect to tumour bulk). Results: Fifty-one scans were included of which 28 had at least one CMB. The majority of CMBs were localized in the lobar area and in deep and periventricular white matter (DPWM) - generally in WM. Only few CMBs were found in GM. In scans obtained up to 7 years after RT completion the majority of CMBs were not colocalized with FLAIR hyperintensities. Conclusion: CMBs and FLAIR hyperintensities appear to be separate imaging biomarkers for radiation therapy induced microvascular damage, as they are not colocalized in patients with LGG, especially not early on after completion of RT