Influence of internal disorder on the superconducting state in the organic layered superconductor kappa-(BEDT-TTF)2Cu[N(CN)2]Br

We report high-sensitivity AC susceptibility measurements of the penetration depth in the Meissner state of the layered organic superconductor kappa-(BEDT-TTF)2Cu[N(CN)2]Br. We have studied nominally pure single crystals from the two different syntheses and employed controlled cooling procedures in order to minimize intrinsic remnant disorder at low temperatures associated with the glass transition, caused by ordering of the ethylene moieties in BEDT-TTF molecule at T_G = 75 K. We find that the optimal cooling procedures (slow cooling of -0.2 K/h or annealing for 3 days in the region of T_G) needed to establish the ground state, depend critically on the sample origin indicating different relaxation times of terminal ethylene groups. We show that, in the ground state, the behavior observed for nominally pure single crystals from both syntheses is consistent with unconventional d-wave order parameter. The in-plane penetration depth lambda_in(T) is strongly linear, whereas the out-of-plane component lambda_out(T) varies as T^2. In contrast, the behavior of single crystals with long relaxation times observed after slow (-0.2 K/h) cooling is as expected for a d-wave superconductor with impurities (i.e. lambda_in(T) propto lambda_out(T) propto T^2) or might be also reasonably well described by the s-wave model. Our results might reconcile the contradictory findings previously reported by different authors.Comment: 13 pages, 10 figures, submitted to Phys. Rev.

Viral pathogenesis, modulation of immune receptor signaling and treatment.

During the co-evolution of viruses and their hosts, the latter have equipped themselves with an elaborate immune system to defend themselves from the invading viruses. In order to establish a successful infection, replicate and persist in the host, viruses have evolved numerous strategies to counter and evade host antiviral immune responses as well as exploit them for productive viral replication. These strategies include those that target immune receptor transmembrane signaling. Uncovering the exact molecular mechanisms underlying these critical points in viral pathogenesis will not only help us understand strategies used by viruses to escape from the host immune surveillance but also reveal new therapeutic targets for antiviral as well as immunomodulatory therapy. In this chapter, based on our current understanding of transmembrane signal transduction mediated by multichain immune recognition receptors (MIRRs) and the results of sequence analysis, we discuss the MIRR-targetingviral strategies of immune evasion and suggest their possible mechanisms that, in turn, reveal new points of antiviral intervention. We also show how two unrelated enveloped viruses, human immunodeficiency virus and human cytomegalovirus, use a similar mechanism to modulate the host immune response mediated by two functionally different MIRRs-T-cell antigen receptor and natural killer cell receptor, NKp30. This suggests that it is very likely that similar general mechanisms can be or are used by other viral and possibly nonviral pathogens