56 research outputs found
'Mind the Gap' in Fitness-For-Service Assessment Procedures-Review and Summary of a Recent Workshop
The influence of temperature on hydrogen environmentally assisted cracking of AA7449-T7651 in moist air
Development of a microstructural cohesive zone model for intergranular hydrogen environmentally assisted cracking
Mecanismos moleculares involucrados en el control de la expresión génica y el desarrollo tumoral
Además de diversos procesos fisiológicos que controlan el desarrollo tumoral, existen mecanismos moleculares por los cuales se determina el destino de una célula. Estos mecanismos permiten la proliferación de las células que el organismo detecta como sanas o normales o bien, ante daños genómicos que no pudieron ser reparados y el riesgo de expansión de estos errores, las células son eliminadas por apoptosis o entran en estado de senescencia replicativa. El correcto funcionamiento de estos mecanismos es el que garantiza el estado de salud del individuo.Fil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto de Investigaciones Medicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Micenmacher, Sabrina Mariel. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto de Investigaciones Medicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Rubio, Maria Fernanda. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto de Investigaciones Medicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Fernandez Larrosa, Pablo Nicolas. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto de Investigaciones Medicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentin
3D characterisation of hydrogen environmentally assisted cracking during static loading of AA7449-T7651
In this investigation, synchrotron X-ray microtomography was used to perform 3D in situ observations of crack initiation and growth during hydrogen environmentally assisted cracking (HEAC) in tensile samples of AA7449-T7651. Two smooth tensile samples with a 1 mm diameter gauge section were held at a fixed displacement (≈30% of yield stress) in warm, moist air (≈76∘C, 73% relative humidity). The samples were then imaged repeatedly using X-ray tomography until they fractured completely. The tomograms showing the nucleation and evolution of intergranular cracks were correlated with electron microscopy fractographs. This enabled the identification of crack initiation sites and the characterisation of the crack growth behaviour relative to the microstructure. The samples were found to fracture within an environmental exposure time of 240 min. Some cracks in both samples nucleated within an exposure time of 80 min (33–40% of the total lifetime). Many cracks were found to nucleate both internally and at the sample surface. However, only superficial cracks contributed to the final fracture surface as they grew faster owing to the direct environmental exposure and the larger crack opening. HEAC occurred prominently via brittle intergranular cracking, and cracks were found to slow down when approaching grain boundary triple junctions. Additionally, crack shielding from nearby cracks and the presence of coarse Al–Cu–Fe particles at the grain boundaries were also found to temporarily reduce the crack growth rates. After prolonged crack growth, the HEAC cracks displayed ductile striations and transgranular fracture, revealing a change in the crack growth mechanism at higher stress intensity factors
RAC3 overexpression is a transforming and proliferative signal that contributes to tumoral development
RAC3 fue caracterizado originalmente como un coactivador de receptores nucleares que se encuentra en cantidades limitantes en células normales, aunque sobreexpresado en tumores y es además coactivador de NF-кB. Si bien se desconocen los mecanismos involucrados en el aumento de su expresión, se sabe que induce resistencia a apoptosis. En este trabajo se investigó si RAC3 podrÃa contribuir al desarrollo tumoral por otros mecanismos y si la citoquina TNF-α, que se encuentra en alto tÃtulo en pacientes con cáncer, podrÃa favorecer el aumento en la expresión de RAC3. Se observó que el aumento en la expresión del coactivador por transfección de células no tumorales de riñón embrionario humano HEK293 no solo aumenta significativamente la proliferación en presencia de suero, sino además en ausencia de factores de crecimiento. También se indujo la transformación celular dando un fenotipo con crecimiento independiente de anclaje similar a lo observado para células tumorales. El tratamiento de las células HEK293 en cultivo con TNF-α indujo un aumento en los niveles proteicos de RAC3 respecto de las células sin estÃmulo y este efecto fue inhibido por pretratamiento con un inhibidor especÃfico de la activación de NF-кB, indicando que la activación de este factor de transcripción está involucrada en la acción de la citoquina. Se concluye que RAC3, además de su acción anti-apoptótica, es un factor transformante que promueve la proliferación y el crecimiento independiente de anclaje, cuyos niveles podrÃan ser aumentados en la tumorigénesis, probablemente vÃa las citoquinas inflamatorias involucradas en la respuesta anti-tumoral.RAC3 has been firstly characterized as a nuclear receptor coactivator that is found in limited amounts in normal cells, but is over-expressed in tumors and is also an NF-кB coactivator. Although the mechanisms involved in its over-expression are not clear, it is well known that it enhances resistance to apoptosis. In this work, we investigated if there are any additional mechanisms by which RAC3 may contribute to tumor development and if TNF-α, an inflammatory cytokine that is found at high levels in cancer could increase RAC3 levels. We found that enhancement of RAC3 levels by transfection of HEK293 cells with a RAC3 expression vector induces a significant increase of cell proliferation not only in the presence, but also in the absence of serum growth factors. Moreover, the cells were transformed showing an anchorage independent growth, similar to that observed in tumoral cells. The treatment of HEK293 cells with TNF-α induced an increase in the protein levels of RAC3 and this was blocked by an NF-кB specific inhibitor, suggesting that this transcription factor is involved in the cytokine effect. We conclude that RAC3, in addition to is anti-apoptotic action, is a transforming factor that promotes the proliferation and growth independent of anchorage, and that its levels could be elevated by the action of inflammatory cytokines that are involved in the anti-tumoral response.Fil: Alvarado, Cecilia Viviana. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto de Investigaciones Medicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Micenmacher, Sabrina Mariel. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto de Investigaciones Medicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Ruiz Grecco, Marina. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto de Investigaciones Medicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Rubio, Maria Fernanda. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto de Investigaciones Medicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Fernandez Larrosa, Pablo Nicolas. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto de Investigaciones Medicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto de Investigaciones Medicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentin
Corrosion mechanisms of plasma welded Nickel aluminium bronze immersed in seawater
Nickel Aluminium Bronzes (NAB) are copper-based multi-phase alloys used extensively in marine applications. NAB is vulnerable to seawater corrosion, however the interaction between its corrosion mechanisms and real-world factors including biofouling, weld microstructure and residual stress are poorly understood. Seawater corrosion tests were performed on plasma-welded NAB in laboratory and marine environments, demonstrating that the retained β’ phase in the Heat Affected Zone (HAZ) experiences Selective Phase Corrosion (SPC), whereas crevice corrosion associated with SPC of the κIII phase occurs at biofouled and stressed areas of parent material. These factors, seldom simulated in physical tests, severely impact NAB’s corrosion resistance.The authors acknowledge the support of ANSTO in providing access to instruments, capabilities and facilities used in this via Proposal 13838. This work was supported by the EPSRC [grant number EP/R513179/1] and Babcock International [studentship number 2019 - 4720]
- …