New Parameterization in Muon Decay and the Type of Emitted Neutrino

Normal muon decay, $\mu^{+} \to e^{+}\nu_{e}\bar{\nu_{\mu}}$, is studied as a tool to discriminate between the Dirac and Majorana types of neutrinos and to survey the structure of the weak interaction. It is assumed that massive neutrinos mix with one another and that the interaction Hamiltonian consists of the $V-A$ and $V+A$ charged currents. A new set of parameters used in place of the Michel parameters is proposed for the positron distribution. Explicit forms of these new parameters are obtained by assuming that the masses are less than 10 eV for light neutrinos and sufficiently large for heavy Majorana neutrinos, which are not emitted in the muon decay. It is shown that a possible method to discriminate between the Dirac and Majorana cases is to use a characterization given by the $\chi^2$ fitting of their spectra. It is also confirmed that the theoretical predictions in the Majorana neutrino case are almost the same as those obtained from the standard model. Indeed, their differences cannot be distinguished within the present experimental precision.Comment: 30 page

A posteriori error estimates for discontinuous Galerkin Methods for the Generalised Korteweg-de Vries Equation

We construct, analyze and numerically validate a posteriori error estimates for conservative discontinuous Galerkin (DG) schemes for the Generalized Korteweg-de Vries (GKdV) equation. We develop the concept of dispersive reconstruction, i.e., a piecewise polynomial function which satisfies the GKdV equation in the strong sense but with a computable forcing term enabling the use of a priori error estimation techniques to obtain computable upper bounds for the error. Both semidiscrete and fully discrete approximations are treated

Structural Modeling of HIV-1 Env-gp120

Variable V1/V2 and V3 loops on human immunodeficiency virus type 1 (HIV-1) envelope-gp120 core play key roles in modulating viral competence to recognize two infection receptors, CD4 and chemokine-receptors. However, molecular bases for the modulation largely remain unclear. To address these issues, we constructed structural models for a full-length gp120 in CD4-free and -bound states. The models showed topologies of gp120 surface loop that agree with those in reported structural data. Molecular dynamics simulation showed that in the unliganded state, V1/V2 loop settled into a thermodynamically stable arrangement near V3 loop for conformational masking of V3 tip, a potent neutralization epitope. In the CD4-bound state, however, V1/V2 loop was rearranged near the bound CD4 to support CD4 binding. In parallel, cell-based adaptation in the absence of anti-viral antibody pressures led to the identification of amino acid substitutions that individually enhance viral entry and growth efficiencies in association with reduced sensitivity to CCR5 antagonist TAK-779. Notably, all these substitutions were positioned on the receptors binding surfaces in V1/V2 or V3 loop. In silico structural studies predicted some physical changes of gp120 by substitutions with alterations in viral replication phenotypes. These data suggest that V1/V2 loop is critical for creating a gp120 structure that masks co-receptor binding site compatible with maintenance of viral infectivity, and for tuning a functional balance of gp120 between immune escape ability and infectivity to optimize HIV-1 replication fitness

In silico Analysis of HIV-1 Env-gp120 Reveals Structural Bases for Viral Adaptation in Growth-Restrictive Cells

Variable V1/V2 and V3 loops on human immunodeficiency virus type 1 (HIV-1) envelope-gp120 core play key roles in modulating viral competence to recognize two infection receptors, CD4 and chemokine-receptors. However, molecular bases for the modulation largely remain unclear. To address these issues, we constructed structural models for a full-length gp120 in CD4-free and -bound states. The models showed topologies of gp120 surface loop that agree with those in reported structural data. Molecular dynamics simulation showed that in the unliganded state, V1/V2 loop settled into a thermodynamically stable arrangement near V3 loop for conformational masking of V3 tip, a potent neutralization epitope. In the CD4-bound state, however, V1/V2 loop was rearranged near the bound CD4 to support CD4 binding. In parallel, cell-based adaptation in the absence of anti-viral antibody pressures led to the identification of amino acid substitutions that individually enhance viral entry and growth efficiencies in association with reduced sensitivity to CCR5 antagonist TAK-779. Notably, all these substitutions were positioned on the receptors binding surfaces in V1/V2 or V3 loop. In silico structural studies predicted some physical changes of gp120 by substitutions with alterations in viral replication phenotypes. These data suggest that V1/V2 loop is critical for creating a gp120 structure that masks co-receptor binding site compatible with maintenance of viral infectivity, and for tuning a functional balance of gp120 between immune escape ability and infectivity to optimize HIV-1 replication fitness

Analysis of Adaptive Mutations in HIV-1 Env-gp120

HIV-1 Env protein functions in the entry process and is the target of neutralizing antibodies. Its intrinsically high mutation rate is certainly one of driving forces for persistence/survival in hosts. For optimal replication in various environments, HIV-1 Env must continue to adapt and evolve through balancing sometimes incompatible function, replication fitness, and neutralization sensitivity. We have previously reported that adapted viruses emerge in repeated and prolonged cultures of cells originally infected with a macaque-tropic HIV-1NL4-3 derivative. We have also shown that the adapted viral clones exhibit enhanced growth potentials both in macaque PBMCs and individuals, and that three single-amino acid mutations are present in their Env V1/C2/C4 domains. In this study, we investigated how lab-adapted and highly neutralization-sensitive HIV-1NL4-3 adapts its Env to macaque cells with strongly replication-restrictive nature for HIV-1. While a single and two mutations gave a significantly enhanced replication phenotype in a macaque cell line and also in human cell lines that stably express either human CD4 or macaque CD4, the virus simultaneously carrying the three adaptive mutations always grew best. Entry kinetics of parental and triple mutant viruses were similar, whereas the mutant was significantly more readily inhibited for its infectivity by soluble CD4 than parental virus. Furthermore, molecular dynamics simulations of the Env ectodomain (gp120 and gp41 ectodomain) bound with CD4 suggest that the three mutations increase binding affinity of Env for CD4 in solution. Thus, it is quite likely that the affinity for CD4 of the mutant Env is enhanced relative to the parental Env. Neutralization sensitivity of the triple mutant to CD4 binding site antibodies was not significantly different from that of parental virus, whereas the mutant exhibited a considerably higher resistance against neutralization by a CD4-induced epitope antibody and Env trimer-targeting V1/V2 antibodies. These results suggest that the three adaptive mutations cooperatively promote viral growth via increased CD4 affinity, and also that they enhance viral resistance to several neutralization antibodies by changing the Env-trimer conformation. In total, we have verified here an HIV-1 adaptation pathway in host cells and individuals involving Env derived from a lab-adapted and highly neutralization-sensitive clone

Pixel Color Clustering of Multi-Temporally Acquired Digital Photographs of a Rice Canopy by Luminosity-Normalization and Pseudo-Red-Green-Blue Color Imaging

Red-green-blue (RGB) channels of RGB digital photographs were loaded with luminosity-adjusted R, G, and completely white grayscale images, respectively (RGwhtB method), or R, G, and R + G (RGB yellow) grayscale images, respectively (RGrgbyB method), to adjust the brightness of the entire area of multi-temporally acquired color digital photographs of a rice canopy. From the RGwhtB or RGrgbyB pseudocolor image, cyan, magenta, CMYK yellow, black, L*, a*, and b* grayscale images were prepared. Using these grayscale images and R, G, and RGB yellow grayscale images, the luminosity-adjusted pixels of the canopy photographs were statistically clustered. With the RGrgbyB and the RGwhtB methods, seven and five major color clusters were given, respectively. The RGrgbyB method showed clear differences among three rice growth stages, and the vegetative stage was further divided into two substages. The RGwhtB method could not clearly discriminate between the second vegetative and midseason stages. The relative advantages of the RGrgbyB method were attributed to the R, G, B, magenta, yellow, L*, and a* grayscale images that contained richer information to show the colorimetrical differences among objects than those of the RGwhtB method. The comparison of rice canopy colors at different time points was enabled by the pseudocolor imaging method