Modelling and analysis of a metal hydride cooling system

Abstract

The work which is presented by J. Payá Herrero, titled "Modelling and analysis of a metal hydride cooling system" has been carried out at the Institute for Energy Engineering under my supervision and assessment.As the modelling and experimental objectives have been reached, I authorise the submission of this PhD work for its evaluation by the corresponding examination board. This PhD thesis consists in the modelling and validation of a metal hydride cooling system. The experimental prototype is located in the institute IKE.In the first place, the hydrogen absorbing materials have been characterized in terms of the static P-C-T properties and of the intrinsic reaction kinetics. In the second place, after this first characterization phase, a completely dynamic model has been developed based on the heat and mass transfer processes which take place in the reactors. The results have been validated with an exhaustive experimental campaign of dynamic cooling tests and the adjustment of the model is very good.Finally, the cooling performance of the system has been improved by means of the model which has enabled the optimization of the operating conditions and of the sorption materials. El presente estudio consiste en el modelado y validación de un sistema de producción de frío basado en la absorción/desorción de hidrógeno en metales.La instalación experimental que se ha modelado se halla en el instituto IKE.En primer lugar, los materiales utilizados se han caracterizado tanto desde el punto de vista de las curvas P-C-T de equilibrio como de la cinética de absorción/desorción de cada aleación. En segundo lugar, se ha desarrollado un modelo completamente dinámico basado en las reacciones de transferencia de calor y masa que ocurren en los reactores. Los resultados se han validado con una amplia gama de medidas de IKE en régimen transitorio, obteniendo un ajuste muy bueno para diferentes ensayos.Finalmente, mediante la utilización del modelo, se han optimizado las condiciones de operación y las propiedades de los materiales, alcanzando así mejores prestaciones en refrigeración.

Relationship between IκBα constitutive expression, TNFα synthesis, and apoptosis in EBV-infected lymphoblastoid cells

“…Supershift experiment evidenced both p65/p50 and p50 2 complexes (Figure 1), which is consistent with previous reports (Herrero et al, 1995). No NF-kB binding activity was detected in IkBa transfected clones, which indicated that both p65/ p50 and p50 2 complexes were apparently inhibited by IkBa.…”

“…Moreover, transfection of IkBa has been shown to induce a relocalization of p50 into the cytoplasm (Zabel et al, 1993). Finally, p105 gene expression is regulated by NF-kB (Ten et al, 1992) and LMP1 induces p105 through NF-kB activation (Herrero et al, 1995). Since our EMSA experiments were done on nuclear extracts, the lack of detection of any Rel/NFkB complexes in our transfected clones may be explained by three hypothesis which are not exclusive: (i) IkBa may translocate in the nucleus (ArenzanaSeisdedos et al, 1995;Cressman and Taub, 1993;Zabel et al, 1993) where it inhibits the DNA binding of Rel/ NF-kB complexes with an e cacy related to its di erential a nity to these complexes; (ii) IkBa may relocate Rel/NF-kB complexes into the cytoplasm, including p50 2 complexes and (iii) the constitutive expression of the stably transfected mutated IkBa 32/36A may down regulate the p105 gene transcription leading to a decrease in the total amount of some Rel/NF-kB proteins such as p50.…”

“…However, natural variants of LMP1 from EBV isolates still have the capacity to activate NF-kB, even if mutations or deletions are occurring within the NF-kB activation domain, suggesting that it exerts a selective pressure on EBV strains to keep intact the capacity of NF-kB activation through the LMP1 proteins in EBV-infected B-cells (Rothenberger et al, 1997). LMP1 activation of NF-kB corresponds to the translocation of p65/p50 complexes in the nucleus, and targets IkBa phosphorylation and degradation, and over-expression of IkBa inhibits the NF-kB activation by LMP1 (Herrero et al, 1995). Therefore, IkBa expressing vectors could be an interesting tool in controlling NF-kB activity and thus, to understand the relationships between EBV-induced transformation and NF-kB activation.…”

Epstein-Barr virus latent membrane protein-1 (LMP1) C-terminus activation region 2 (CTAR2) maps to the far C-terminus and requires oligomerisation for NF-κB activation

“…The lower blot was probed with the OX34 monoclonal antibody that recognises the rCD2 extracellular domain other proteins. Whilst phosphorylation and subsequent degradation of IkB is the most likely mechanism of activation of NF-kB by LMP1 (Herrero et al, 1995), the means by which CTAR1 and CTAR achieve this presumably di er, and the exact role of TRAFs and other associated proteins in this process remains to be elucidated. Although the necessity of LMP1 oligomerisation to activate signal transduction was predicted from the known association of TRAFs with the CTAR1 domain, we also show that CTAR2-mediated NF-kB activation similarly requires the physical interaction of several LMP1 molecules.…”

Epstein–Barr virus latent membrane protein-1 (LMP1) signalling is distinct from CD40 and involves physical cooperation of its two C-terminus functional regions

“…Whilst both CD40 and LMP1 are reported to activate p50/RelA heterodimers (Herrero et al, 1995;Rothe et al, 1995) it is not clear that this is su cient to activate CD54 gene expression; it has been reported that RelA/cRel heterodimers may play a crucial role in CD54 gene expression (Ledebur and Parks, 1995). Alternatively, or in addition, it is possible that other signalling pathways such as the SEK/JNK/AP1 pathway (Reinhard et al, 1997) normally activated by the association of TRAF2 with members of the TNFreceptor superfamily, or even the MAPK pathway (Roberts and Cooper, 1998), are involved in regulation of CD54 gene expression and may be selectively impaired in Jurkat T cells but not in Eli-BL cells.…”