Anatomy of Bs→PVB_s \to PV decays and effects of next-to-leading order contributions in the perturbative QCD factorization approach

In this paper, we will make systematic calculations for the branching ratios and the CP-violating asymmetries of the twenty one $\bar{B}^0_s \to PV$ decays by employing the perturbative QCD (PQCD) factorization approach. Besides the full leading-order (LO) contributions, all currently known next-to-leading order (NLO) contributions are taken into account. We found numerically that: (a) the NLO contributions can provide $\sim 40\%$ enhancement to the LO PQCD predictions for ${\cal B}(\bar{B}_s^0 \to K^0 \bar{K}^{*0})$ and ${\cal B}(\bar{B}_s^0 \to K^{\pm}K^{*\mp})$, or a $\sim 37\%$ reduction to \calb(\bar{B}_s^0 \to \pi^{-} K^{*+}), and we confirmed that the inclusion of the known NLO contributions can improve significantly the agreement between the theory and those currently available experimental measurements, (b) the total effects on the PQCD predictions for the relevant $B\to P$ transition form factors after the inclusion of the NLO twist-2 and twist-3 contributions is generally small in magnitude: less than $10\%$ enhancement respect to the leading order result, (c) for the "tree" dominated decay $\bar B_s^0\to K^+ \rho^-$ and the "color-suppressed-tree" decay $\bar B_s^0\to \pi^0 K^{*0}$, the big difference between the PQCD predictions for their branching ratios are induced by different topological structure and by interference effects among the decay amplitude ${\cal A}_{T,C}$ and ${\cal A}_P$: constructive for the first decay but destructive for the second one, and (d) for \bar{B}_s^0 \to V(\eta, \etar) decays, the complex pattern of the PQCD predictions for their branching ratios can be understood by rather different topological structures and the interference effects between the decay amplitude \cala(V\eta_q) and \cala(V\eta_s) due to the \eta-\etar mixing.Comment: 18 pages, 2 figures, 3 tables. Some modifications of the text. Several new references are adde

Dirac fermions with plaquette interactions. III. SU(N) phase diagram with Gross-Neveu criticality and first-order phase transition

Inspired by our recent works[1, 2] of SU(2) and SU(4) Dirac fermions subjected to plaquette interactions on square lattice, here we extend the large-scale quantum Monte Carlo investigations to the phase digram of correlated Dirac fermions with SU(6) and SU(8) symmetries subjected to the plaquette interaction on the same lattice. From SU(2) to SU(8), the rich phase diagram exhibits a plethora of emerging quantum phases such as the Dirac semimetal, the antiferromagnetic Mott insulator, valence bond solid (VBS) and the Dirac spin liquid and phase transitions including the Gross-Neveu chiral transitions with emergent continuous symmetry, the deconfined quantum criticality and the first order transition between interaction-driven columnar VBS and plaquette VBS. These rich phenomena coming from the simple-looking lattice models, firmly convey the message that the interplay between the $SU(N)$ Dirac fermions -- with enhanced internal symmetries -- and extended plaquette interactions -- beyond the on-site Hubbard type -- is the new playground to synthesise novel highly entangled quantum matter both at the model level and with experimental feasibilities.Comment: 9 pages, 7 figure

Caution on Gross-Neveu criticality with a single Dirac cone: Violation of locality and its consequence of unexpected finite-temperature transition

Lately there are many SLAC fermion investigations on the (2+1)D Gross-Neveu criticality of a single Dirac cone [1,2]. While the SLAC fermion construction indeed gives rise to the linear energy-momentum relation for all lattice momenta at the non-interacting limit, the long-range hopping and its consequent violation of locality on the Gross-Neveu quantum critical point (GN-QCP) -- which a priori requires short-range interaction -- has not been verified. Here we show, by means of large-scale quantum Monte Carlo simulations, that the interaction-driven antiferromagnetic insulator in this case is fundamentally different from that on a purely local $\pi$-flux Hubbard model on the square lattice. In particular, we find the antiferromagnetic long-range order in the SLAC fermion model has a finite temperature continuous phase transition, which violates the Mermin-Wagner theorem, and smoothly connects to the previously determined GN-QCP. The magnetic excitations inside the antiferromagnetic insulator are gapped without Goldstone mode, even though the state spontaneously breaks continuous $SU(2)$ symmetry. These unusual results proclaim caution on the interpretation of the quantum phase transition in SLAC fermion model as that of GN-QCP with short-range interaction

Dirac fermions with plaquette interactions. I. SU(2) phase diagram with Gross-Neveu and deconfined quantum criticalities

We investigate the ground state phase diagram of an extended Hubbard model with $\pi$-flux hopping term at half-filling on a square lattice, with unbiased large-scale auxiliary-field quantum Monte Carlo simulations. As a function of interaction strength, there emerges an intermediate phase which realizes two interaction-driven quantum critical points, with the first between the Dirac semimetal and an insulating phase of weak valence bond solid (VBS) order, and the second separating the VBS order and an antiferromagnetic insulating phase. These intriguing quantum critical points are respectively bestowed with Gross-Neveu and deconfined quantum criticalities, and the critical exponents $\eta_\text{VBS}=0.6(1)$ and $\eta_\text{AF}=0.58(3)$ at deconfined quantum critical point satisfy the CFT Bootstrap bound. We also investigate the dynamical properties of the spin excitation and find the spin gap open near the first transition and close at the second. The relevance of our findings in realizing deconfined quantum criticality in fermion systems and the implication to lattice models with further extended interactions such as those in quantum Moir\'e systems, are discussed.Comment: 6+2 pages, 5+2 figure

8-Benzoyl-7-hy­droxy-4-methyl-2H-1-benzopyran-2-one monohydrate

In the title compound, C17H12O4·H2O, the coumarin ring system is approximately planar with a maximum atomic deviation of 0.011 (2) Å, and is nearly perpendicular to the phenyl ring at a dihedral angle of 86.63 (9)°. In the crystal, mol­ecules are linked by classical O—H⋯O and weak C—H⋯O hydrogen bonds. π–π stacking is also present [centroid–centroid distance = 3.6898 (12) Å]

The First Insight into the Tissue Specific Taxus Transcriptome via Illumina Second Generation Sequencing

The First Insight into the Tissue Specific Taxus Transcriptome via Illumina Second Generation SequencingBackground: Illumina second generation sequencing is now an efficient route for generating enormous sequence collections that represent expressed genes and quantitate expression level. Taxus is a world-wide endangered gymnosperm genus and forms an important anti-cancer medicinal resource, but the large and complex genomes of Taxus have hindered the development of genomic resources. The research of its tissue-specific transcriptome is absent. There is also no study concerning the association between the plant transcriptome and metabolome with respect to the plant tissue type

Carboxylesterase-2 is a highly sensitive target of the antiobesity agent orlistat with profound implications in the activation of anticancer prodrugs

Orlistat has been the most used anti-obesity drug and the mechanism of its action is to reduce lipid absorption by inhibiting gastrointestinal lipases. These enzymes, like carboxylesterases (CESs), structurally belong to the α/β hydrolase fold superfamily. Lipases and CESs are functionally related as well. Some CESs (e.g., human CES1) have been shown to hydrolyze lipids. This study was designed to test the hypothesis that orlistat inhibits CESs with higher potency toward CES1 than CES2, a carboxylesterase with little lipase activity. Liver microsomes and recombinant CESs were tested for the inhibition of the hydrolysis of standard substrates and the anticancer prodrugs pentyl carbamate of p-aminobenzyl carbamate of doxazolidine (PPD) and irinotecan. Contrary to the hypothesis, orlistat at 1 nM inhibited CES2 activity by 75% but no inhibition on CES1, placing CES2 one of the most sensitive targets of orlistat. The inhibition varied among some CES2 polymorphic variants. Pretreatment with orlistat reduced the cell killing activity of PPD. Certain mouse but not rat CESs were also highly sensitive. CES2 is responsible for the hydrolysis of many common drugs and abundantly expressed in the gastrointestinal track and liver. Inhibition of this carboxylesterase probably presents a major source for altered therapeutic activity of these medicines if co-administered with orlistat. In addition, orlistat has been linked to various types of organ toxicities, and this study provides an alternative target potentially involved in these toxicological responses

Hypolipidemic agent Z-guggulsterone: metabolism interplays with induction of carboxylesterase and bile salt export pump

Z-Guggulsterone is a major ingredient in the Indian traditional hypolipidemic remedy guggul. A study in mice has established that its hypolipidemic effect involves the farnesoid X receptor (FXR), presumably by acting as an antagonist of this receptor. It is generally assumed that the antagonism leads to induction of cytochrome P450 7A1 (CYP7A1), the rate-limiting enzyme converting free cholesterol to bile acids. In this study, we tested whether Z-guggulsterone indeed induces human CYP7A1. In addition, the expression of cholesteryl ester hydrolase CES1 and bile salt export pump (BSEP) was monitored. Contrary to the general assumption, Z-guggulsterone did not induce CYP7A1. Instead, this phytosterol significantly induced CES1 and BSEP through transactivation. Z-Guggulsterone underwent metabolism by CYP3A4, and the metabolites greatly increased the induction potency on BSEP but not on CES1. BSEP induction favors cholesterol elimination, whereas CES1 involves both elimination and retention (probably when excessively induced). Interestingly, clinical trials reported the hypolipidemic response rates from 18% to 80% and showed that higher dosages actually increased VLDL cholesterol. Our findings predict that better hypolipidemic outcomes likely occur in individuals who have a relatively higher capacity of metabolizing Z-guggulsterone with moderate CES1 induction, a scenario possibly achieved by lowering the dosing regimens