The Patterns of High-Level Magnetic Activity Occurring on the Surface of V1285 Aql: The OPEA Model of Flares and DFT Models of Stellar Spots

Statistically analyzing Johnson UBVR observations of V1285 Aql during the three observing seasons, both activity level and behavior of the star are discussed in respect to obtained results. We also discuss the out-of-flare variation due to rotational modulation. Eighty-three flares were detected in the U-band observations of season 2006 . First, depending on statistical analyses using the independent samples t-test, the flares were divided into two classes as the fast and the slow flares. According to the results of the test, there is a difference of about 73 s between the flare-equivalent durations of slow and fast flares. The difference should be the difference mentioned in the theoretical models. Second, using the one-phase exponential association function, the distribution of the flare-equivalent durations versus the flare total durations was modeled. Analyzing the model, some parameters such as plateau, half-life values, mean average of the flare-equivalent durations, maximum flare rise, and total duration times are derived. The plateau value, which is an indicator of the saturation level of white-light flares, was derived as 2.421{\pm}0.058 s in this model, while half-life is computed as 201 s. Analyses showed that observed maximum value of flare total duration is 4641 s, while observed maximum flare rise time is 1817 s. According to these results, although computed energies of the flares occurring on the surface of V1285 Aql are generally lower than those of other stars, the length of its flaring loop can be higher than those of more active stars.Comment: 44 pages, 10 figures, 5 tables, 2011PASP..123..659

The Mechanisms of Codon Reassignments in Mitochondrial Genetic Codes

Many cases of non-standard genetic codes are known in mitochondrial genomes. We carry out analysis of phylogeny and codon usage of organisms for which the complete mitochondrial genome is available, and we determine the most likely mechanism for codon reassignment in each case. Reassignment events can be classified according to the gain-loss framework. The gain represents the appearance of a new tRNA for the reassigned codon or the change of an existing tRNA such that it gains the ability to pair with the codon. The loss represents the deletion of a tRNA or the change in a tRNA so that it no longer translates the codon. One possible mechanism is Codon Disappearance, where the codon disappears from the genome prior to the gain and loss events. In the alternative mechanisms the codon does not disappear. In the Unassigned Codon mechanism, the loss occurs first, whereas in the Ambiguous Intermediate mechanism, the gain occurs first. Codon usage analysis gives clear evidence of cases where the codon disappeared at the point of the reassignment and also cases where it did not disappear. Codon disappearance is the probable explanation for stop to sense reassignments and a small number of reassignments of sense codons. However, the majority of sense to sense reassignments cannot be explained by codon disappearance. In the latter cases, by analysis of the presence or absence of tRNAs in the genome and of the changes in tRNA sequences, it is sometimes possible to distinguish between the Unassigned Codon and Ambiguous Intermediate mechanisms. We emphasize that not all reassignments follow the same scenario and that it is necessary to consider the details of each case carefully.Comment: 53 pages (45 pages, including 4 figures + 8 pages of supplementary information). To appear in J.Mol.Evo

Production of crystallizable human chymase from a Bacillus subtilis system

AbstractA Bacillus subtilis strain deficient in seven extracellular proteases was used to produce human mast cell chymase and is a viable expression system for serine proteases and other classes of proteins. Chymase is produced at 0.3–0.5 mg/l and is purified by three chromatography steps. Two crystal forms of PMSF-treated chymase were optimized. The first is C2 with a=47.94 Å, b=85.23 Å, c=174.18 Å, β=96.74°, and diffracts to at least 2.1 Å, while the second is P212121, with cell dimensions a=43.93 Å, b=58.16 Å, and c=86.09 Å, and a diffraction limit of approximately 1.9 Å. The first crystal form has either three or four molecules/asymmetric unit, while the second has one molecule/asymmetric unit

The HgMn Binary Star Phi Herculis: Detection and Properties of the Secondary and Revision of the Elemental Abundances of the Primary

Observations of the Mercury-Manganese star Phi Herculis with the Navy Prototype Optical Interferometer (NPOI) conclusively reveal the previously unseen companion in this single-lined binary system. The NPOI data were used to predict a spectral type of A8V for the secondary star Phi Her B. This prediction was subsequently confirmed by spectroscopic observations obtained at the Dominion Astrophysical Observatory. Phi Her B is rotating at 50 +/-3 km/sec, in contrast to the 8 km/sec lines of Phi Her A. Recognizing the lines from the secondary permits one to separate them from those of the primary. The abundance analysis of Phi Her A shows an abundance pattern similar to those of other HgMn stars with Al being very underabundant and Sc, Cr, Mn, Zn, Ga, Sr, Y, Zr, Ba, Ce, and Hg being very overabundant.Comment: Accepted to ApJ, 45 pages, 11 figure

Stops making sense: translational trade-offs and stop codon reassignment

Background Efficient gene expression involves a trade-off between (i) premature termination of protein synthesis; and (ii) readthrough, where the ribosome fails to dissociate at the terminal stop. Sense codons that are similar in sequence to stop codons are more susceptible to nonsense mutation, and are also likely to be more susceptible to transcriptional or translational errors causing premature termination. We therefore expect this trade-off to be influenced by the number of stop codons in the genetic code. Although genetic codes are highly constrained, stop codon number appears to be their most volatile feature. Results In the human genome, codons readily mutable to stops are underrepresented in coding sequences. We construct a simple mathematical model based on the relative likelihoods of premature termination and readthrough. When readthrough occurs, the resultant protein has a tail of amino acid residues incorrectly added to the C-terminus. Our results depend strongly on the number of stop codons in the genetic code. When the code has more stop codons, premature termination is relatively more likely, particularly for longer genes. When the code has fewer stop codons, the length of the tail added by readthrough will, on average, be longer, and thus more deleterious. Comparative analysis of taxa with a range of stop codon numbers suggests that genomes whose code includes more stop codons have shorter coding sequences. Conclusions We suggest that the differing trade-offs presented by alternative genetic codes may result in differences in genome structure. More speculatively, multiple stop codons may mitigate readthrough, counteracting the disadvantage of a higher rate of nonsense mutation. This could help explain the puzzling overrepresentation of stop codons in the canonical genetic code and most variants

Effects of partially dismantling the CD4 binding site glycan fence of HIV-1 envelope glycoprotein trimers on neutralizing antibody induction

Previously, VLPs bearing JR-FL strain HIV-1 Envelope trimers elicited potent neutralizing antibodies (nAbs) in 2/8 rabbits PLoS Pathog 11(5): e1004932) by taking advantage of a naturally absent glycan at position 197 that borders the CD4 binding site (CD4bs). In new immunizations, we attempted to improve nAb responses by removing the N362 glycan that also lines the CD4bs. All 4 rabbits developed nAbs. One targeted the N197 glycan hole like our previous sera. Two sera depended on the N463 glycan, again suggesting CD4bs overlap. Heterologous boosts appeared to reduce nAb clashes with the N362 glycan. The fourth serum targeted a N362 glycan-sensitive epitope. VLP manufacture challenges prevented us from immunizing larger rabbit numbers to empower a robust statistical analysis. Nevertheless, trends suggest that targeted glycan removal may improve nAb induction by exposing new epitopes and that it may be possible to modify nAb speciUcity using rational heterologous boosts

Reciprocal Roles for CCAAT/Enhancer Binding Protein (C/EBP) and PU.1 Transcription Factors in Langerhans Cell Commitment

Myeloid progenitor cells give rise to a variety of progenies including dendritic cells. However, the mechanism controlling the diversification of myeloid progenitors into each progeny is largely unknown. PU.1 and CCAAT/enhancing binding protein (C/EBP) family transcription factors have been characterized as key regulators for the development and function of the myeloid system. However, the roles of C/EBP transcription factors have not been fully identified because of functional redundancy among family members. Using high titer–retroviral infection, we demonstrate that a dominant-negative C/EBP completely blocked the granulocyte–macrophage commitment of human myeloid progenitors. Alternatively, Langerhans cell (LC) commitment was markedly facilitated in the absence of tumor necrosis factor (TNF)α, a strong inducer of LC development, whereas expression of wild-type C/EBP in myeloid progenitors promoted granulocytic differentiation, and completely inhibited TNFα-dependent LC development. On the other hand, expression of wild-type PU.1 in myeloid progenitors triggered LC development in the absence of TNFα, and its instructive effect was canceled by coexpressed C/EBP. Our findings establish reciprocal roles for C/EBP and PU.1 in LC development, and provide new insight into the molecular mechanism of LC development, which has not yet been well characterized

Afatinib for an elderly patient with chronic kidney disease

Letter to the edito