Coarsening of Disordered Quantum Rotors under a Bias Voltage

We solve the dynamics of an ensemble of interacting rotors coupled to two leads at different chemical potential letting a current flow through the system and driving it out of equilibrium. We show that at low temperature the coarsening phase persists under the voltage drop up to a critical value of the applied potential that depends on the characteristics of the electron reservoirs. We discuss the properties of the critical surface in the temperature, voltage, strength of quantum fluctuations and coupling to the bath phase diagram. We analyze the coarsening regime finding, in particular, which features are essentially quantum mechanical and which are basically classical in nature. We demonstrate that the system evolves via the growth of a coherence length with the same time-dependence as in the classical limit, $R(t) \simeq t^{1/2}$ -- the scalar curvature driven universality class. We obtain the scaling function of the correlation function at late epochs in the coarsening regime and we prove that it coincides with the classical one once a prefactor that encodes the dependence on all the parameters is factorized. We derive a generic formula for the current flowing through the system and we show that, for this model, it rapidly approaches a constant that we compute.Comment: 53 pages, 12 figure

Intracellular expression of Tat alters mitochondrial functions in T cells: a potential mechanism to understand mitochondrial damage during HIV-1 replication

HIV-1 replication results in mitochondrial damage that is enhanced during antiretroviral therapy (ART). The onset of HIV-1 replication is regulated by viral protein Tat, a 101-residue protein codified by two exons that elongates viral transcripts. Although the first exon of Tat (aa 1–72) forms itself an active protein, the presence of the second exon (aa 73–101) results in a more competent transcriptional protein with additional functions. Results: Mitochondrial overall functions were analyzed in Jurkat cells stably expressing full-length Tat (Tat101) or one-exon Tat (Tat72). Representative results were confirmed in PBLs transiently expressing Tat101 and in HIV-infected Jurkat cells. The intracellular expression of Tat101 induced the deregulation of metabolism and cytoskeletal proteins which remodeled the function and distribution of mitochondria. Tat101 reduced the transcription of the mtDNA, resulting in low ATP production. The total amount of mitochondria increased likely to counteract their functional impairment. These effects were enhanced when Tat second exon was expressed. Conclusions: Intracellular Tat altered mtDNA transcription, mitochondrial content and distribution in CD4+ T cells. The importance of Tat second exon in non-transcriptional functions was confirmed. Tat101 may be responsible for mitochondrial dysfunctions found in HIV-1 infected patients.We greatly appreciate the secretarial assistance of Mrs Olga Palao. This work was supported by FIPSE (360924/10), Spanish Ministry of Economy and Competitiveness (SAF2010-18388), Spanish Ministry of Health (EC11- 285), AIDS Network ISCIII-RETIC (RD12/0017/0015), Instituto de Salud Carlos III, Spanish Ministry of Economy and Competitiveness (FIS PI12/00506). The work of Sara Rodríguez-Mora is supported by a fellowship of Sara Borrell from Spanish Ministry of Economy and Competitiveness (2013). The work of María Rosa López-Huertas is supported by a fellowship of the European Union Programme Health 2009 (CHAARM).S