Protecting dissipative quantum state preparation via dynamical decoupling

We show that dissipative quantum state preparation processes can be protected against qubit dephasing by interlacing the state preparation control with dynamical decoupling (DD) control consisting of a sequence of short $\pi$-pulses. The inhomogeneous broadening can be suppressed to second order of the pulse interval, and the protection efficiency is nearly independent of the pulse sequence but determined by the average interval between pulses. The DD protection is numerically tested and found to be efficient against inhomogeneous dephasing on two exemplary dissipative state preparation schemes that use collective pumping to realize many-body singlets and linear cluster states respectively. Numerical simulation also shows that the state preparation can be efficiently protected by $\pi$-pulses with completely random arrival time. Our results make possible the application of these state preparation schemes in inhomogeneously broadened systems. DD protection of state preparation against dynamical noises is also discussed using the example of Gaussian noise with a semiclasscial description.Comment: 9 pages, 8 figure

Unified covariant treatment of hyperfine splitting for heavy and light mesons

This paper aims at proving the fundamental role of a relativistic formulation for quarkonia models. We present a completely covariant description of a two-quark system interacting by the Cornell potential with a Breit term describing the hyperfine splitting. Using an appropriate procedure to calculate the Breit correction, we find heavy meson masses in excellent agreement with experimental data. Moreover, also when applied to light quarks and even taking average values of the running coupling constant, we prove that covariance properties and hyperfine splitting are sufficient to explain the light mesons spectrum and to give a very good agreement with the data.Comment: 4 page

Extended Holographic dark energy

The idea of relating the infrared and ultraviolet cutoffs is applied to Brans-Dicke theory of gravitation. We find that extended holographic dark energy from the Hubble scale or the particle horizon as the infrared cutoff will not give accelerating expansion. The dynamical cosmological constant with the event horizon as the infrared cutoff is a viable dark energy model.Comment: one reference is corrected, 3 pages, no figure,V3: minor correction

Single-Particle Tunneling in Doped Graphene-Insulator-Graphene Junctions

The characteristics of tunnel junctions formed between n- and p-doped graphene are investigated theoretically. The single-particle tunnel current that flows between the two-dimensional electronic states of the graphene (2D-2D tunneling) is evaluated. At a voltage bias such that the Dirac points of the two electrodes are aligned, a large resonant current peak is produced. The magnitude and width of this peak is computed, and its use for devices is discussed. The influence of both rotational alignment of the graphene electrodes and structural perfection of the graphene is discussed.Comment: 23 pages, 9 figures; added Section II(E) and associated figures, and made other minor typographical correction

Upregulation of Functional Kv11.1 Isoform Expression by Inhibition of Intronic Polyadenylation with Antisense Morpholino Oligonucleotides

The KCNH2 gene encodes the Kv11.1 potassium channel that conducts the rapidly activating delayed rectifier current in the heart. KCNH2 pre-mRNA undergoes alternative processing; intron 9 splicing leads to the formation of a functional, full-length Kv11.1a isoform, while polyadenylationwithin intron 9 generates a non-functional, Cterminally truncated Kv11.1a-USO isoform. The relative expression of Kv11.1 isoforms plays an important role in the regulation of Kv11.1 channel function and the pathogenesis of long QT syndrome. In this study,we identified cis-acting elements that are required for KCNH2 intron 9 poly(A) signal activity. Mutation of these elements decreased Kv11.1a-USO expression and increased the expression of Kv11.1a mRNA, protein and channel current. More importantly, blocking these elements by antisense morpholino oligonucleotides shifted the alternative processing of KCNH2 intron 9 from the polyadenylation to the splicing pathway, leading to the predominant production of Kv11.1a and a significant increase in Kv11.1 current. Our findings indicate that the expression of the Kv11.1a isoform can be upregulated by an antisense approach. Antisense inhibition of KCNH2 intronic polyadenylation represents a novel approach to increase Kv11.1 channel function

Upregulation of Functional Kv11.1a Isoform Expression by Modified U1 Small Nuclear RNA

The KCNH2 or human ether-a go-go-related gene (hERG) encodes the Kv11.1 potassium channel that conducts the rapidly activating delayed rectifier potassium current in the heart. The expression of Kv11.1 C-terminal isoforms is directed by the alternative splicing and polyadenylation of intron 9. Splicing of intron 9 leads to the formation of a functional, full-length Kv11.1a isoform and polyadenylation of intron 9 results in the production of a non-functional, C-terminally truncated Kv11.1a-USO isoform. The relative expression of Kv11.1a and Kv11.1a-USO plays an important role in regulating Kv11.1 channel function. In the heart, only one-third of KCNH2 pre-mRNA is processed to Kv11.1a due to the weak 5′ splice site of intron 9. We previously showed that the weak 5′ splice site is caused by sequence deviation from the consensus, and that mutations toward the consensus sequence increased the efficiency of intron 9 splicing. It is well established that 5′ splice sites are recognized by complementary base-paring with U1 small nuclear RNA (U1 snRNA). In this study, we modified the sequence of U1 snRNA to increase its complementarity to the 5′ splice site of KCNH2 intron 9 and observed a significant increase in the efficiency of intron 9 splicing. RNase protection assay and western blot analysis showed that modified U1 snRNA increased the expression of the functional Kv11.1a isoform and concomitantly decreased the expression of the non-functional Kv11.1a-USO isoform. In patch-clamp experiments, modified U1 snRNA significantly increased Kv11.1 current. Our findings suggest that relative expression of Kv11.1 C-terminal isoforms can be regulated by modified U1 snRNA

Position of Premature Termination Codons Determines Susceptibility of hERG Mutations to Nonsense-Mediated mRNA Decay in Long QT Syndrome

The degradation of human ether-a-go-go-related gene (hERG, KCNH2) transcripts containing premature termination codon (PTC)mutations by nonsense-mediatedmRNA decay (NMD) is an importantmechanismof long QT syndrome type 2 (LQT2). The mechanisms governing the recognition of PTC-containing hERG transcripts asNMD substrates have not been established. We used a minigene system to study two frameshift mutations, R1032Gfs*25 and D1037Rfs*82. R1032Gfs*25 introduces a PTC in exon 14, whereas D1037Rfs*82 causes a PTC in the last exon (exon 15). We showed that R1032Gfs*25, but not D1037Rfs*82, reduced the level of mutant mRNA compared to thewild-type minigene in an NMD-dependent manner. The deletion of intron 14 prevented degradation of R1032Gfs*25 mRNA indicating that a downstream intron is required for NMD. The recognition and elimination of PTC-containing transcripts by NMD required that the mutation be positioned N54–60 nt upstream of the 3′-most exon–exon junction. Finally, we used a full-length hERG splicing-competent construct to show that inhibition of downstream intron splicing by antisense morpholino oligonucleotides inhibited NMD and rescued the functional expression of a third LQT2 mutation, Y1078*. The present study defines the positional requirements for the susceptibility of LQT2mutations toNMD and posits that the majority of reported LQT2 nonsense and frameshift mutations are potential targets of NMD

Upregulation of Functional Kv11.1 Isoform Expression by Inhibition of Intronic Polyadenylation with Antisense Morpholino Oligonucleotides

The KCNH2 gene encodes the Kv11.1 potassium channel that conducts the rapidly activating delayed rectifier current in the heart. KCNH2 pre-mRNA undergoes alternative processing; intron 9 splicing leads to the formation of a functional, full-length Kv11.1a isoform, while polyadenylationwithin intron 9 generates a non-functional, Cterminally truncated Kv11.1a-USO isoform. The relative expression of Kv11.1 isoforms plays an important role in the regulation of Kv11.1 channel function and the pathogenesis of long QT syndrome. In this study,we identified cis-acting elements that are required for KCNH2 intron 9 poly(A) signal activity. Mutation of these elements decreased Kv11.1a-USO expression and increased the expression of Kv11.1a mRNA, protein and channel current. More importantly, blocking these elements by antisense morpholino oligonucleotides shifted the alternative processing of KCNH2 intron 9 from the polyadenylation to the splicing pathway, leading to the predominant production of Kv11.1a and a significant increase in Kv11.1 current. Our findings indicate that the expression of the Kv11.1a isoform can be upregulated by an antisense approach. Antisense inhibition of KCNH2 intronic polyadenylation represents a novel approach to increase Kv11.1 channel function

In-flight boundary-layer measurements on a hollow cylinder at a Mach number of 3.0

Skin temperatures, shear forces, surface static pressures, boundary layer pitot pressures, and boundary layer total temperatures were measured on the external surface of a hollow cylinder that was 3.04 meters long and 0.437 meter in diameter and was mounted beneath the fuselage of the YF-12A airplane. The data were obtained at a nominal free stream Mach number of 3.0 (a local Mach number of 2.9) and at wall to recovery temperature ratios of 0.66 to 0.91. The local Reynolds number had a nominal value of 4,300,000 per meter. Heat transfer coefficients and skin friction coefficients were derived from skin temperature time histories and shear force measurements, respectively. In addition, boundary layer velocity profiles were derived from pitot pressure measurements, and a Reynolds analogy factor was obtained from the heat transfer and skin friction measurements. The measured data are compared with several boundary layer prediction methods

In-flight Compressible Turbulent Boundary Layer Measurements on a Hollow Cylinder at a Mach Number of 3.0

Skin temperatures, shearing forces, surface static pressures, and boundary layer pitot pressures and total temperatures were measured on a hollow cylinder 3.04 meters long and 0.437 meter in diameter mounted beneath the fuselage of the YF-12A airplane. The data were obtained at a nominal free stream Mach number of 3.0 and at wall-to-recovery temperature ratios of 0.66 to 0.91. The free stream Reynolds number had a minimal value of 4.2 million per meter. Heat transfer coefficients and skin friction coefficients were derived from skin temperature time histories and shear force measurements, respectively. Boundary layer velocity profiles were derived from pitot pressure measurements, and a Reynolds analogy factor of 1.11 was obtained from the measured heat transfer and skin friction data. The skin friction coefficients predicted by the theory of van Driest were in excellent agreement with the measurements. Theoretical heat transfer coefficients, in the form of Stanton numbers calculated by using a modified Reynolds analogy between skin friction and heat transfer, were compared with measured values. The measured velocity profiles were compared to Coles' incompressible law-of-the-wall profile