La ética hacker frente al capitalismo netárquíco: software libre y peer production en las iniciativas de Economía Colaborativa en Andalucía

En los últimos años el término Economía Colaborativa se ha popularizado sin que, hasta el momento, haya sido definido de manera inequívoca. Bajo esta denominación se engloban experiencias tan diversas como bancos de tiempo, huertos urbanos, startups o grandes plataformas digitales. La proliferación de este tipo de iniciativas puede relacionarse con una multiplicidad de factores tales como el desarrollo tecnológico, la recesión económica y otras crisis superpuestas (medioambiental, de cuidados, de valores, de lo político) y un cierto cambio en los valores sociales. Entre 2014-2015 se han realizado dos investigaciones en Andalucía de manera casi paralela y con una metodología similar. La primera de ellas pretendía identificar prácticas de Economía Colaborativa en el entorno universitario. La segunda investigación identificaba experiencias de emprendimiento a nivel autonómico. A luz de los resultados obtenidos se plantea la siguiente cuestión sobre la naturaleza misma de la Economía Colaborativa: ¿nos encontramos ante prácticas postcapitalistas que abren el camino a una sociedad más justa e igualitaria o, más bien, estamos ante una respuesta del capital para, una vez más, seguir extrayendo de manera privada el valor que se genera socialmente? Este artículo, partiendo del análisis del conjunto de iniciativas detentadas en Andalucía, se centra en aquellas basadas en el software libre y la producción digital concluyendo cómo, gracias a la incorporación de ciertos aspectos de la ética hacker y las lógicas del conocimiento abierto, éstas pueden situarse dentro de un escenario de fomento de los comunes globales frente a las lógicas imperantes del capitalismo netárquico. 

Teoria da arte hacker : estética, diferença e transgressão tecnológica

Tese (doutorado)—Universidade de Brasília, Instituto de Artes, Departamento de Artes Visuais, Programa de Pós-Graduação em Arte, 2015.

La ética hacker: marco para la disrupción educativa de la "universidad zombi"

La crisis actual de la educación es, ante todo, una crisis de las instituciones y su filosofía,señala Bauman(2007: 148),por eso en este trabajo vamos a centrarnos en la ética que afecta a una institución educativa: la universidad. No vamos a hablar, por tanto, del futuro, sino del presente, caracterizadoprecisamente por el «desmantelamiento de marcos y liquidación de pautas» (Bauman, 2007: 145) que producen la sensación de «fin de ciclo». Efectivamente, la idea de que vivimos momentos de cambios profundos es recurrente en el pensamiento contemporáneo occidental. No hay más que repasar someramente las etiquetas acuñadas para testimoniar el cambio de paradigmas: sociedad líquida (Bauman), sociedad red, de la información y del conocimiento (Castells), posmodernidad (Bell), sobremodernidad (Augé), modernidad tardía (Giddens), era tecnotrónica (Brzezinski), tercera ola (Toffler), sociedad de la incultura (Mayos), era del acceso (Watts)o civilización empática (Rifkin)son sólo algunos de los términos que, si bien fijan la atención en diversos componentes y los explican desde diferentes disciplinas y épocas, coinciden, sin embargo, en señalar aspectos comunes de dichos cambios. ¿Cómo afectan estas trasformaciones a la universidad y a la educación en general?

Enhancement of DNA repair using topical T4 endonuclease V does not inhibit melanoma formation in Cdk4R24C/R24C/Tyr-NrasQ61K mice following neonatal UVR

To further investigate the use of DNA repair-enhancing agents for skin cancer prevention, we treated Cdk4R24C/R24C/NrasQ61K mice topically with the T4 endonuclease V DNA repair enzyme (known as Dimericine) immediately prior to neonatal ultraviolet radiation (UVR) exposure, which has a powerful effect in exacerbating melanoma development in the mouse model. Dimericine has been shown to reduce the incidence of basal-cell and squamous cell carcinoma. Unexpectedly, we saw no difference in penetrance or age of onset of melanoma after neonatal UVR between Dimericine-treated and control animals, although the drug reduced DNA damage and cellular proliferation in the skin. Interestingly, epidermal melanocytes removed cyclobutane pyrimidine dimers (CPDs) more efficiently than surrounding keratinocytes. Our study indicates that neonatal UVR-initiated melanomas may be driven by mechanisms other than solely that of a large CPD load and/or their inefficient repair. This is further suggestive of different mechanisms by which UVR may enhance the transformation of keratinocytes and melanocytes.

Differential roles of the pRb and Arf/p53 pathways in murine naevus and melanoma genesis

We report on a systematic analysis of genotype-specific melanocyte (MC) UVR responses in transgenic mouse melanoma models along with tumour penetrance and comparative histopathology. pRb or p53 pathway mutations cooperated with NrasQ61K to transform MCs. We previously reported that MCs migrate from the follicular outer root sheath into the epidermis after neonatal UVR. Here, we found that Arf or p53 loss markedly diminished this response. Despite this, mice carrying these mutations developed melanoma with very early age of onset after neonatal UVR. Cdk4R24C did not affect the MC migration. Instead, independent of UVR exposure, interfollicular dermal MCs were more prevalent in Cdk4R24C mice. Subsequently, in adulthood, these mutants developed dermal MC proliferations reminiscent of superficial congenital naevi. Two types of melanoma were observed in this model. The location and growth pattern of the first was consistent with derivation from the naevi, while the second appeared to be of deep dermal origin. In animals carrying the Arf or p53 defects, no naevi were detected, with all tumours ostensibly skipping the benign precursor stage in progression.

The association between MC1R genotype and BRAF mutation status in cutaneous melanoma : findings from an Australian population

There is increasing epidemiological and molecular evidence that cutaneous melanomas arise through multiple causal pathways. The purpose of this study was to explore the relationship between germline and somatic mutations in a population-based series of melanoma patients to reshape and refine the divergent pathway model for melanoma. Melanomas collected from 123 Australian patients were analyzed for melanocortin-1 receptor (MC1R) variants and mutations in the BRAF and NRAS genes. Detailed phenotypic and sun exposure data were systematically collected from all patients. We found that BRAF-mutant melanomas were significantly more likely from younger patients and those with high nevus counts, and were more likely in melanomas with adjacent neval remnants. Conversely, BRAF-mutant melanomas were significantly less likely in people with high levels of lifetime sun exposure. We observed no association between germline MC1R status and somatic BRAF mutations in melanomas from this population. BRAF-mutant melanomas have different origins from other cutaneous melanomas. These data support the divergent pathways hypothesis for melanoma, which may require a reappraisal of targeted cancer prevention activities.

Melanocyte homeostasis in vivo tolerates Rb1 loss in a developmentally independent fashion

There has been uncertainty regarding the precise role that the pocket protein Rb1 plays in murine melanocyte homeostasis. It has been reported that the TAT-Cre mediated loss of exon 19 from a floxed Rb1 allele causes melanocyte apoptosis in vivo and in vitro. This is at variance with other findings showing, either directly or indirectly, that Rb1 loss in melanocytes has no noticeable effect in vivo, but in vitro leads to a semi-transformed phenotype. In this study, we show that Rb1-null melanocytes lacking exon 19 do not undergo apoptosis and survive both in vitro and in vivo, irrespective of the developmental stage at which Cre-mediated ablation of the exon occurs. Further, Rb1 loss has no serious long-term ramifications on melanocyte homeostasis in vivo, with Rb1-null melanocytes being detected in the skin after numerous hair cycles, inferring that the melanocyte stem cell population carrying the Cre-mediated deletion is maintained. Consequently, whilst Rb1 loss in the melanocyte is able to alter cellular behaviour in vitro, it appears inconsequential with respect to melanocyte homeostasis in the mouse skin.

Inverse expression states of the BRN2 and MITF transcription factors in melanoma spheres and tumour xenografts regulate the NOTCH pathway

The use of adherent monolayer cultures have produced many insights into melanoma cell growth and differentiation, but often novel therapeutics demonstrated to act on these cells are not active in vivo. It is imperative that new methods of growing melanoma cells that reflect growth in vivo are investigated. To this end, a range of human melanoma cell lines passaged as adherent cultures or induced to form melanoma spheres (melanospheres) in stem cell media have been studied to compare cellular characteristics and protein expression. Melanoma spheres and tumours grown from cell lines as mouse xenografts had increased heterogeneity when compared with adherent cells and 3D-spheroids in agar (aggregates). Furthermore, cells within the melanoma spheres and mouse xenografts each displayed a high level of reciprocal BRN2 or MITF expression, which matched more closely the pattern seen in human melanoma tumours in situ, rather than the propensity for co-expression of these important melanocytic transcription factors seen in adherent cells and 3D-spheroids. Notably, when the levels of the BRN2 and MITF proteins were each independently repressed using siRNA treatment of adherent melanoma cells, members of the NOTCH pathway responded by decreasing or increasing expression, respectively. This links BRN2 as an activator, and conversely, MITF as a repressor of the NOTCH pathway in melanoma cells. Loss of the BRN2-MITF axis in antisense-ablated cell lines decreased the melanoma sphere-forming capability, cell adhesion during 3D-spheroid formation and invasion through a collagen matrix. Combined, this evidence suggests that the melanoma sphere-culture system induces subpopulations of cells that may more accurately portray the in vivo disease, than the growth as adherent melanoma cells.