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A bstract It has been shown recently that the anomalies observed in B ¯ → D * τ ν ¯ τ and B ¯ → K ¯ ℓ + ℓ − decays could be resolved with just one scalar leptoquark. Fitting to the current data on R ( D (∗)) along with acceptable q 2 distributions in B ¯ → D ∗ τ ν ¯ τ decays, four best-fit solutions for the operator coefficients have been found. In this paper, we explore the possibilities of how to discriminate these four solutions. Firstly, we find that two of them are already excluded by the decay B c − → τ − ν ¯ τ , because the predicted decay widths have already overshot the total width Γ B c . It is then found that the remaining two solutions result in two effective Hamiltonians governing b → c τ ν ¯ τ transition, which differ by a sign and enhance the absolute value of the coefficient of c ¯ L γ μ b L τ ¯ L γ μ ν τ L operator by about 12%. However, they give nearly the same predictions as in the SM for the D ∗ and τ longitudinal polarizations as well as the lepton forward-backward asymmetries in B ¯ → D ∗ τ ν ¯ τ decays. For the other observables like ℬ B c − → τ − ν ¯ τ , ℬ B c − → γ τ − ν ¯ τ , R D ∗ q 2 , d ℬ B ¯ → D ∗ τ ν ¯ τ / d q 2 and ℬ B c − → X 3 τ ν ¯ τ , on the other hand, the two solutions give sizable enhancements relative to the SM predictions. With measurement of B c − → τ − ν ¯ τ at LHCb and refined measurements of observables in B ¯ → D ∗ τ ν ¯ τ at both LHCb and Belle-II, such a specific NP scenario could be further deciphered.

A bstract With the hypothesis of minimal flavor violation, we find that there exists a power-aligned relation between the Yukawa couplings of the two scalar doublets in the two-Higgs-doublet model with Hermitian Yukawa matrices. Within such a power-aligned framework, it is found that a simultaneous explanation of the anomalies observed in the electron and muon anomalous magnetic moments can be reached with TeV-scale quasi-degenerate Higgs masses, and the resulting parameter space is also phenomenologically safer under the B-physics, Z and τ decay data, as well as the current LHC bounds. Furthermore, the flavor-universal power that enhances the charged-lepton Yukawa couplings prompts an interesting correlation between the two anomalies, which makes the model distinguishable from the (generalized) linearly aligned and the lepton-specific two-Higgs-doublet models that address the same anomalies but in a non-correlative manner, and hence testable by future precise measurements.

A bstract We complete the calculation of the QCD penguin amplitude at next-to-next- to-leading order in the QCD factorization approach to non-leptonic B -meson decays. This provides the last missing piece in the computation of the QCD correction to direct CP asymmetries at leading power in the heavy-quark expansion.

Many in vitro studies have shown that tea catechins had vevarious health beneficial effects. However, inconsistent results between in vitro and in vivo studies or between laboratory tests and epidemical studies are observed. Low bioavailability of tea catechins was an important factor leading to these inconsistencies. Research advances in bioavailability studies involving absorption and metabolic biotransformation of tea catechins were reviewed in the present paper. Related techniques for improving their bioavailability such as nanostructure-based drug delivery system, molecular modification, and co-administration of catechins with other bioactives were also discussed.

A bstract With updated experimental data and improved theoretical calculations, several significant deviations are being observed between the Standard Model predictions and the experimental measurements of the branching ratios of B ¯ s 0 → D s ∗ + L − decays, where L is a light meson from the set { π , ρ , K (∗) }. Especially for the two channels B ¯ 0 → D + K − and B ¯ s 0 → D s + π − , both of which are free of the weak annihilation contribution, the deviations observed can even reach 4–5 σ . Here we exploit possible new-physics effects in these class-I non-leptonic B -meson decays within the framework of QCD factorization. Firstly, we perform a model-independent analysis of the effects from twenty linearly independent four-quark operators that can contribute, either directly or through operator mixing, to the quark-level b → c u ¯ d s transitions. It is found that, under the combined constraints from the current experimental data, the deviations observed could be well explained at the 1 σ level by the new-physics four-quark operators with γ μ (1 − γ 5 ) ⨂ γ μ (1 − γ 5 ) structure, and also at the 2 σ level by the operators with (1 + γ 5 ) ⨂ (1 − γ 5 ) and (1 + γ 5 ) ⨂ (1 + γ 5 ) structures. However, the new-physics four-quark operators with other Dirac structures fail to provide a consistent interpretation, even at the 2 σ level. Then, as two specific examples of model-dependent considerations, we discuss the case where the new-physics four-quark operators are generated by either a colorless charged gauge boson or a colorless charged scalar, with their masses fixed both at the 1 TeV. Constraints on the effective coefficients describing the couplings of these mediators to the relevant quarks are obtained by fitting to the current experimental data.

• Secondary growth is a key characteristic of trees, which requires the coordination of multiple regulatory mechanisms including transcriptional regulators and microRNAs (miRNAs). However, the roles of microRNAs in the regulation of secondary growth need to be explored in depth. • Here, the role of miR319a and its target, PtoTCP20, in the secondary growth of Populus tomentosa stem was investigated using genetic and molecular analyses. • The expression level of miR319a gradually decreased from primary to secondary growth in P. tomentosa, while that of PtoTCP20 gradually increased. MiR319a overexpression in seedlings resulted in delayed secondary growth and decreased xylem production, while miR319a knockdown and PtoTCP20 overexpression promoted secondary growth and increased xylem production. Further analysis showed that PtoTCP20 interacted with PtoWOX4a and activated PtoWND6 transcription in vitro and in vivo. • Our data show that PtoTCP20 controls vascular cambium proliferation by binding to PtoWOX4a, and promotes secondary xylem differentiation by activating PtoWND6 transcription, thereby regulating secondary growth in P. tomentosa. Our findings provide insight into the molecular mechanisms underlying secondary growth in trees.

(–)-Epigallocatechin-3-O-gallate (EGCG), the most abundant component of catechins in tea (Camellia sinensis (L.) O. Kuntze), plays a role against viruses through inhibiting virus invasiveness, restraining gene expression and replication. In this paper, the antiviral effects of EGCG on various viruses, including DNA virus, RNA virus, coronavirus, enterovirus and arbovirus, were reviewed. Meanwhile, the antiviral effects of the EGCG epi-isomer counterpart (+)-gallocatechin-3-O-gallate (GCG) were also discussed.

Volatile compounds are important components of tea aroma, a key attribute of sensory quality. The present review examines the formation of aromatic volatiles of various kinds of teas and factors influencing the formation of tea volatiles, including tea cultivar, growing environment and agronomic practices, processing method and storage of tea. The determination of tea volatiles and the relationship of active-aroma volatiles with the sensory qualities of tea are also discussed in the present paper.

Background Handelin is a bioactive compound from Chrysanthemum indicum L. that improves motor function and muscle integrity during aging in Caenorhabditis elegans. This study aimed to further evaluate the protective effects and molecular mechanisms of handelin in a mouse muscle atrophy model induced by cachexia and aging. Methods A tumour necrosis factor (TNF)‐α‐induced atrophy model was used to examine handelin activity in cultured C2C12 myotubes in vitro. Lipopolysaccharide (LPS)‐treated 8‐week‐old model mice and 23‐month‐old (aged) mice were used to examine the therapeutic effects of handelin on cachexia‐ and aging‐induced muscle atrophy, respectively, in vivo. Protein and mRNA expressions were analysed by Western blotting, ELISA and quantitative PCR, respectively. Skeletal muscle mass was measured by histological analysis. Results Handelin treatment resulted in an upregulation of protein levels of early (MyoD and myogenin) and late (myosin heavy chain, MyHC) differentiation markers in C2C12 myotubes (P < 0.05), and enhanced mitochondrial respiratory (P < 0.05). In TNF‐α‐induced myotube atrophy model, handelin maintained MyHC protein levels, increased insulin‐like growth factor (Igf1) mRNA expression and phosphorylated protein kinase B protein levels (P < 0.05). Handelin also reduced atrogin‐1 expression, inhibited nuclear factor‐κB activation and reduced mRNA levels of interleukin (Il)6, Il1b and chemokine ligand 1 (Cxcl1) (P < 0.05). In LPS‐treated mice, handelin increased body weight (P < 0.05), the weight (P < 0.01) and cross‐sectional area (CSA) of the soleus muscle (P < 0.0001) and improved motor function (P < 0.05). In aged mice, handelin slightly increased the weight of the tibialis anterior muscle (P = 0.06) and CSA of the tibialis anterior and gastrocnemius muscles (P < 0.0001). In the tibialis anterior muscle of aged mice, handelin upregulated mRNA levels of Igf1 (P < 0.01), anti‐inflammatory cytokine Il10 (P < 0.01), mitochondrial biogenesis genes (P < 0.05) and antioxidant‐related enzymes (P < 0.05) and strengthened Sod and Cat enzyme activity (P < 0.05). Handelin also reduced lipid peroxidation and protein carbonylation, downregulated mRNA levels of Fbxo32, Mstn, Cxcl1, Il1b and Tnf (P < 0.05), and decreased IL‐1β levels in serum (P < 0.05). Knockdown of Hsp70 or using an Hsp70 inhibitor abolished the ameliorating effects of handelin on myotube atrophy. Conclusions Handelin ameliorated cachexia‐ and aging‐induced skeletal muscle atrophy in vitro and in vivo, by maintaining homeostasis of protein synthesis and degradation, possibly by inhibiting inflammation. Handelin is a potentially promising drug candidate for the treatment of muscle wasting.

A bstract We evaluate in the framework of QCD factorization the two-loop vertex corrections to the decays B ¯ s → D s ∗ + L − and Λ b  →  Λ c + L − , where L is a light meson from the set { π, ρ, K (∗) , a 1 }. These decays are paradigms of the QCD factorization approach since only the colour-allowed tree amplitude contributes at leading power. Hence they are sensitive to the size of power corrections once their leading-power perturbative expansion is under control. Here we compute the two-loop O α s 2 correction to the leading-power hard scattering kernels, and give the results for the convoluted kernels almost completely analytically. Our newly computed contribution amounts to a positive shift of the magnitude of the tree amplitude by ∼ 2%. We then perform an extensive phenomenological analysis to NNLO in QCD factorization, using the most recent values for non-perturbative input parameters. Given the fact that the NNLO perturbative correction and updated values for form factors increase the theory prediction for branching ratios, while experimental central values have at the same time decreased, we reanalyze the role and potential size of power corrections by means of appropriately chosen ratios of decay channels.