Dirac-vortex topological photonic crystal fibre

The success of photonic crystal fibres relies largely on the endless variety of two-dimensional photonic crystals in the cross-section. Here, we propose a topological bandgap fibre whose bandgaps along in-plane directions are opened by generalized Kekul\'e modulation of a Dirac lattice with a vortex phase. Then, the existence of mid-gap defect modes is guaranteed to guide light at the core of this Dirac-vortex fibre, where the number of guiding modes equals the winding number of the spatial vortex. The single-vortex design provides a single-polarization single mode for a bandwidth as large as one octave

Space-group theory of photonic bands

The wide-range application of photonic crystals and metamaterials benefits from the enormous design space of three-dimensional sub-wavelength structures. In this work, we study the space group constraints on photonic dispersions for all 230 space groups with time-reversal symmetry. Our theory carefully treats the unique singular point of photonic bands at zero frequency and momentum, which distinguishes photonic bands from their electronic counterpart. The results are given in terms of minimal band connectivities at zero~($M$) and non-zero frequencies~($M'$). Topological band degeneracies are guaranteed to be found in space groups that do not allow band gaps between the second and third photonic bands~($M>2$). Our work provides theoretical guidelines for the choice of spatial symmetries in photonics design

Data_Sheet_1_Mitotic-Spindle Organizing Protein MztA Mediates Septation Signaling by Suppressing the Regulatory Subunit of Protein Phosphatase 2A-ParA in Aspergillus nidulans.PDF

<p>The proper timing and positioning of cytokinesis/septation is crucial for hyphal growth and conidiation in Aspergillus nidulans. The septation initiation network (SIN) components are a conserved spindle pole body (SPB) localized signaling cascade and the terminal kinase complex SidB-MobA, which must localize on the SPB in this pathway to trigger septation/cytokinesis. The regulatory subunit of phosphatase PP2A-ParA has been identified to be a negative regulator capable of inactivating the SIN. However, little is known about how ParA regulates the SIN pathway and whether ParA regulates the septum formation process through affecting the SPB-localized SIN proteins. In this study, through RNA-Seq and genetic approaches, we identified a new positive septation regulator, a putative mitotic-spindle organizing protein and a yeast Mzt1 homolog MztA, which acts antagonistically toward PP2A-ParA to coordinately regulate the SPB-localized SIN proteins SidB-MobA during septation. These findings imply that regulators, phosphatase PP2A-ParA and MztA counteract the septation function probably through balancing the polymerization and depolymerization of microtubules at the SPB.</p

The Evolutionary Rates of HCV Estimated with Subtype 1a and 1b Sequences over the ORF Length and in Different Genomic Regions

<div><p>Background</p><p>Considerable progress has been made in the HCV evolutionary analysis, since the software BEAST was released. However, prior information, especially the prior evolutionary rate, which plays a critical role in BEAST analysis, is always difficult to ascertain due to various uncertainties. Providing a proper prior HCV evolutionary rate is thus of great importance.</p><p>Methods/Results</p><p>176 full-length sequences of HCV subtype 1a and 144 of 1b were assembled by taking into consideration the balance of the sampling dates and the even dispersion in phylogenetic trees. According to the HCV genomic organization and biological functions, each dataset was partitioned into nine genomic regions and two routinely amplified regions. A uniform prior rate was applied to the BEAST analysis for each region and also the entire ORF. All the obtained posterior rates for 1a are of a magnitude of 10⁻³ substitutions/site/year and in a bell-shaped distribution. Significantly lower rates were estimated for 1b and some of the rate distribution curves resulted in a one-sided truncation, particularly under the exponential model. This indicates that some of the rates for subtype 1b are less accurate, so they were adjusted by including more sequences to improve the temporal structure.</p><p>Conclusion</p><p>Among the various HCV subtypes and genomic regions, the evolutionary patterns are dissimilar. Therefore, an applied estimation of the HCV epidemic history requires the proper selection of the rate priors, which should match the actual dataset so that they can fit for the subtype, the genomic region and even the length. By referencing the findings here, future evolutionary analysis of the HCV subtype 1a and 1b datasets may become more accurate and hence prove useful for tracing their patterns.</p></div

The evolutionary rates and tMRCAs estimated for the 1a and 1b datasets in nine genomic regions and over ORF by root-to-tip regression.

¶<p>In the calendar year. <b>*</b> The evolutionary rate is negative and tMRCA locates in the future.</p

The median evolutionary rates and the tMRCAs estimated in the nine genomic regions and over the entire ORF of the subtype 1a and 1b datasets.

<p>Panels A, B, and C show the median evolutionary rates. Panels D, E, and F show the median tMRCAs. The blue columns represent the estimates for 1a. The red columns represent the estimates for 1b. The dash lines indicate the estimates for the entire ORF.</p

The violin plots of the posterior evolutionary rate estimated using the uniform (0, 0.01) rate prior in the nine genomic regions and over the entire ORF of the subtype 1a (A panel) and 1b (B panel) datasets.

<p>Combined with the GTR+I+Γ substitution model and Bayesian skyline coalesent model, the MCMC procedures were run under three clock models, exoponetial, lognormal, and strict, respectively, using BEAST. The vertical axis measures the substitution rate multiplied by 10⁻³ (substitution/site/year). The horizontal axis indicates the nine genomic regions and the entire ORF. The left three panels show the results for the 1a dataset. The right three panels show the results for the 1b dataset. In each panel, two violins are separated in a small case on the right, which indicate the rates estimated for the routinely amplified partial Core-E1 (P-C/E1) and partial NS5B (P-NS5B) regions.</p

Samarium Ion-Promoted Cross-Aldol Reactions and Tandem Aldol/Evans−Tishchenko Reactions

Cross-aldol reactions of carbonyl compounds were achieved by the catalysis of SmI2 or SmI3, together with molecular sieves, at ambient temperature. 1,3-Dichloroacetone and 1-chloroacetone can be used as acceptor substrates in the cross-aldol reactions with donor substrates such as acetone, cyclopentanone, and cyclohexanone. The cross-aldol reactions with (R)-glyceraldehyde acetonide gave optically pure compounds 25−32, the stereochemistry of which was in agreement with a chairlike chelate transition state of dipolar mode. SmI2−molecular sieves or SmI3−molecular sieves also functioned as effective Lewis acids to catalyze tandem aldol/Evans−Tishchenko reactions. The aldol/Evans−Tishchenko reactions of methyl ketones with aldehydes occurred at 0 °C to give α,γ-anti diol monoesters 53a−59a. When the reactions were conducted at room temperature, a certain degree of transesterification took place. The aldol/Evans−Tishchenko reactions of ethyl or benzyl ketones with aldehydes yielded α,β-anti−α,γ-anti diol monoesters 60a−65a. However, the aldol/Evans−Tishchenko reactions of cyclic ketones with benzaldehyde occurred with a different stereoselectivity to give α,β-syn−α,γ-anti diol monoesters 66a−76a. The structures of products were determined by chemical and spectroscopic methods including an X-ray diffraction analysis of 72a derived from the reaction of 4-tert-butylcyclohexanone and benzaldehyde. A reaction mechanism involving dissociation−recombination of aldols followed by intramolecular stereoselective hydride shift is proposed, based on some experimental evidence, to explain the dichotomous stereoselectivity using acyclic or cyclic ketones as the reaction substrates

Samarium Ion-Promoted Cross-Aldol Reactions and Tandem Aldol/Evans−Tishchenko Reactions

Cross-aldol reactions of carbonyl compounds were achieved by the catalysis of SmI2 or SmI3, together with molecular sieves, at ambient temperature. 1,3-Dichloroacetone and 1-chloroacetone can be used as acceptor substrates in the cross-aldol reactions with donor substrates such as acetone, cyclopentanone, and cyclohexanone. The cross-aldol reactions with (R)-glyceraldehyde acetonide gave optically pure compounds 25−32, the stereochemistry of which was in agreement with a chairlike chelate transition state of dipolar mode. SmI2−molecular sieves or SmI3−molecular sieves also functioned as effective Lewis acids to catalyze tandem aldol/Evans−Tishchenko reactions. The aldol/Evans−Tishchenko reactions of methyl ketones with aldehydes occurred at 0 °C to give α,γ-anti diol monoesters 53a−59a. When the reactions were conducted at room temperature, a certain degree of transesterification took place. The aldol/Evans−Tishchenko reactions of ethyl or benzyl ketones with aldehydes yielded α,β-anti−α,γ-anti diol monoesters 60a−65a. However, the aldol/Evans−Tishchenko reactions of cyclic ketones with benzaldehyde occurred with a different stereoselectivity to give α,β-syn−α,γ-anti diol monoesters 66a−76a. The structures of products were determined by chemical and spectroscopic methods including an X-ray diffraction analysis of 72a derived from the reaction of 4-tert-butylcyclohexanone and benzaldehyde. A reaction mechanism involving dissociation−recombination of aldols followed by intramolecular stereoselective hydride shift is proposed, based on some experimental evidence, to explain the dichotomous stereoselectivity using acyclic or cyclic ketones as the reaction substrates

Root-to-tip regression to estimate the tMRCAs and clock rates.

<p>A simple linear regression of the root-to-tip genentic distances against the sampling dates was performed using the Path-o-gen software. The root was determined by maximizing the coefficent of determinant R². The vertical axis measures the genetic distances between the samples and the root while the horizontal axis scales the sampling dates (year). For subtype 1a (A), the mean evolutionary rate (the slope of regression line) is 9.05E-4 substitution/site/year and the tMRCA (the X-intercept) is located at 1941. For subtype 1b (B), the mean evolutionary rate is 4.82E-4 and the tMRCA is located at 1808.</p