Search

We investigate entanglement breaking times of Markovian evolutions in discrete and continuous time. In continuous time, we characterize which Markovian evolutions are eventually entanglement breaking, that is, evolutions for which there is a finite time after which any entanglement initially present has been destroyed by the noisy evolution. In the discrete-time framework, we consider the entanglement breaking index, that is, the number of times a quantum channel has to be composed with itself before it becomes entanglement breaking. The PPT 2 conjecture is that every PPT quantum channel has an entanglement breaking index of at most 2; we prove that every faithful PPT quantum channel has a finite entanglement breaking index, and more generally, any faithful PPT CP map whose Hilbert–Schmidt adjoint is also faithful is eventually entanglement breaking. We also provide a method to obtain concrete bounds on this index for any faithful quantum channel. To obtain these estimates, we use a notion of robustness of separability to obtain bounds on the radius of the largest separable ball around faithful product states. We also extend the framework of Poincaré inequalities for non-primitive semigroups to the discrete setting to quantify the convergence of quantum semigroups in discrete time, which is of independent interest. [ABSTRACT FROM AUTHOR]

We analyse Landauer’s principle for repeated interaction systems consisting of a reference quantum system S in contact with an environment E which is a chain of independent quantum probes. The system S interacts with each probe sequentially, for a given duration, and Landauer’s principle relates the energy variation of E and the decrease of entropy of S by the entropy production of the dynamical process. We consider refinements of the Landauer bound at the level of the full statistics (FS) associated with a two-time measurement protocol of, essentially, the energy of E. The emphasis is put on the adiabatic regime where the environment, consisting of T≫1 probes, displays variations of order T-1 between the successive probes, and the measurements take place initially and after T interactions. We prove a large deviation principle and a central limit theorem as T→∞ for the classical random variable describing the entropy production of the process, with respect to the FS measure. In a special case, related to a detailed balance condition, we obtain an explicit limiting distribution of this random variable without rescaling. At the technical level, we obtain a non-unitary adiabatic theorem generalizing that of Hanson et al. (Commun Math Phys 349(1):285-327, 2017) and analyse the spectrum of complex deformations of families of irreducible completely positive trace-preserving maps. [ABSTRACT FROM AUTHOR]

Melorheostosis is a sporadic disease of uncertain etiology characterized by asymmetric bone overgrowth and functional impairment. Using whole exome sequencing, we identify somatic mosaic MAP2K1 mutations in affected, but not unaffected, bone of eight unrelated patients with melorheostosis. The activating mutations (Q56P, K57E and K57N) cluster tightly in the MEK1 negative regulatory domain. Affected bone displays a mosaic pattern of increased p-ERK1/2 in osteoblast immunohistochemistry. Osteoblasts cultured from affected bone comprise two populations with distinct p-ERK1/2 levels by flow cytometry, enhanced ERK1/2 activation, and increased cell proliferation. However, these MAP2K1 mutations inhibit BMP2-mediated osteoblast mineralization and differentiation in vitro, underlying the markedly increased osteoid detected in affected bone histology. Mosaicism is also detected in the skin overlying bone lesions in four of five patients tested. Our data show that the MAP2K1 oncogene is important in human bone formation and implicate MEK1 inhibition as a potential treatment avenue for melorheostosis. [ABSTRACT FROM AUTHOR]

Introduction: We describe a previously unreported 437 T→G missense mutation producing a V146G substitution in the first coiled-coil (CC1) domain of nuclear factor-κB essential modulator (NEMO) in a 9-month-old boy with ectodermal dysplasia with immunodeficiency who presented with methicillin-resistant Staphylococcus aureus subdural empyema. We performed in vitro experiments to determine if this novel mutation resulted in impaired NF-κB signaling. Methods: IκBα phosphorylation experiments were performed using a Jurkat T cell line lacking endogenous NEMO expression that was transfected with vectors containing either the wild type or the patient's V146G mutation. The cells were stimulated with TNF-α to activate the NF-κB pathway. Phosphorylated IκBα was detected by immunoblotting with anti-phospho-IκBα antibodies. Peripheral blood mononuclear cells from the patient were stimulated with TNF-α or anti-CD3 and anti-CD28. Impaired IκBα degradation was detected using antibodies against the IκBα protein. Results: While TNF-α stimulation resulted in IκBα phosphorylation in NEMO-deficient Jurkat cells reconstituted with wild-type NEMO, cell transfected with the V146G mutant exhibited a 75% reduction in phospho-IκBα. Peripheral blood mononuclear cells from the patient showed impaired degradation of IκBα after stimulation when compared with normal controls. Conclusions: The patient's V146G mutation results in impaired NF-κB activation in vitro. The mutation extends the known N-terminal boundary within the CC1 domain that produces an ectodermal dysplasia phenotype, and defines an infectious susceptibility previously unappreciated in ectodermal dysplasia with immunodeficiency (methicillin-resistant S. aureus subdural empyema), broadening the clinical spectrum associated with the disease. [ABSTRACT FROM AUTHOR]

Signaling through the hematopoietic receptors requires activation of receptor-associated Janus (Jak) kinases. For example, Jak1 and Jak3 bind specifically to the IL-2 receptor beta (IL-2Rβ) and common gamma (γc) chains, respectively, and initiate biochemical signals critical in controlling immune responses. The region of Jak responsible for receptor interactions, however, is not well characterized. Here we describe a naturally occurring Jak3 mutation from a patient with autosomal severe combined immunodeficiency (SCID), where a single amino acid substitution, Y100C, in Janus homology domain 7 (JH7) prevents kinase­receptor interaction. This mutation also results in a loss of IL-2-induced signaling in a B-cell line derived from this patient. Using mutational analysis we have identified a region of Jak3, including portions of JH6 and JH7, that is sufficient for kinase­receptor contact and show that this segment interacts with the proline-rich Box1 region of the receptor. Furthermore, a Jak3­Jak1 chimera containing only the JH6 and JH7 domains of Jak3 interacts with γc and can reconstitute IL-2-dependent responses, including receptor phosphorylation and activation of signal transducer and activator of transcription (STAT) 5b. Our results suggest that the N-terminus of Jak kinases is critical for receptor binding, and is therefore likely to determine specificity of Jak kinase­receptor interactions. [ABSTRACT FROM AUTHOR]