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A bstract Flavor SU(3) symmetry is a powerful tool to analyze charmed baryon decays. In this work, we propose an approach to generate SU(3) sum rules for the singly and doubly charmed baryon decays without writing the Wigner-Eckhart invariants explicitly. The SU(3) sum rules are computed routinely in several master formulas. Hundreds of SU(3) sum rules are found to serve as test of the flavor symmetry in the charmed baryon decays.

Isospin symmetry, as the most precise flavor symmetry, can be used to extract information about hadronic dynamics. The effective Hamiltonian for bottom quark weak decay is zero under the isospin lowering operators I - n , which allows us to generate isospin sum rules through several master formulas. In this work, we derive the master formulas of isospin sum rules for the two- and three-body non-leptonic decays of B mesons. Numerous new isospin sum rules, especially those involving three or more decay channels, are proposed. The isospin sum rules can be used to test isospin symmetry and provide hints the isospin partners of exotic hadrons in B decays. It is found ten percent isospin breaking only in decay modes involving two vector mesons, indicating the complex dynamics of vector mesons. Besides, the isospin analysis suggests the charm tetraquark resonances might be observed in the B - → J / Ψ π - K ¯ 0 , B ¯ 0 → J / Ψ K ¯ 0 ϕ , and B ¯ 0 → D 0 D ¯ 0 K ¯ 0 modes.

A bstract Isospin symmetry is the most precise flavor symmetry. In this work, we propose an approach to generate isospin sum rules for heavy hadron decays without the Wigner-Eckhart invariants. The effective Hamiltonian of heavy quark weak decay is fully invariant under a series of isospin lowering operators I − n and then the isospin sum rules can be generated through several master formulas. It provides a systematic way to study the isospin symmetry of c - and b -hadron weak decays. The theoretical framework of this approach is presented in detail with the nonleptonic decays of D and B mesons as examples. In addition, the V -/ U -spin sum rules are derived in a similar algorithm by replacing I − n with V − n / U − n .

A bstract We proposed a theoretical framework to correlate the topological diagram at quark level and rescattering dynamics at hadron level. In the framework, both the hadronic triangle diagram, and the topological-scattering diagram, which is the intermediate structure between topological diagram and triangle diagram, are expressed in the tensor form. The completeness of topological-scattering diagram is confirmed by the quark substructure of meson-meson scattering. The coefficient of each triangle diagram can be derived from the topological-scattering diagram and the total rescattering amplitudes are consistent with the ones derived from the chiral Lagrangian. If only the short-distance T diagram is considered as the weak vertex in triangle diagram, the rescattering contributions in the C , E and P diagrams have definite proportional relation of L ( C ) : L ( E ) : L ( P ) = − 2 : 1 : 1 under the SU (3) F symmetry, and the rescattering contributions in the T and A diagrams only arise from the SU (3) F breaking effects. Taking D → Kπ and D → ππ modes as examples, we present our framework in detail. We find the Isospin relations in these decays are still valid in terms of triangle diagrams. Besides, the conclusions in the D meson decays under the SU (3) F symmetry can be generalized to the B meson decays under the SU (4) F symmetry.

High gravimetric energy density, earth-abundance, and environmental friendliness of hydrogen sources have inspired the utilization of hydrogen fuel as a clean alternative to fossil fuels. Hydrogen evolution reaction （HER）, a half reaction of water splitting, is crucial to the low-cost production of pure H2 fuels but necessitates the use of electrocatalysts to expedite reaction kinetics. Owing to the availability of low-cost oxygen evolution reaction （OER） catalysts for the counter electrode in alkaline media and the lack of low-cost OER catalysts in acidic media, researchers have focused on developing HER catalysts in alkaline media with high activity and stability. Nickel is well-known as an HER catalyst and continuous efforts have been undertaken to improve Ni-based catalysts as alkaline electrolyzers： In this review, we summarize earlier studies of HER activity and mechanism on Ni surfaces, along with recent progress in the optimization of the Ni-based catalysts using various modern techniques. Recently developed Ni-based HER catalysts are categorized according to their chemical nature, and the advantages as well as limitations of each category are discussed. Among all Ni-based catalysts, Ni-based alloys and Ni-based hetero-structure exhibit the most promising electrocatalytic activity and stability owing to the fine-tuning of their surface adsorption properties via a synergistic nearby element or domain. Finally, selected applications of the developed Ni-based HER catalysts are highlighted, such as water splitting, the chloralkali process, and microbial electrolysis cell.

MicroRNAs (miRNAs) play a critical role in regulation of numerous biological processes and pathogenesis of a variety of diseases. In addition, miRNAs contribute to carcinogenesis by acting as oncogenic or tumor suppressive. Circulating miRNAs including miR-150-5p are associated with colorectal cancer progression, and the putative targets of miR-150-5p include tumor suppressor gene, TP53. Here we sought to investigate the role of miR-150-5p-TP53 signaling pathway in proliferation of colon cancer and to determine expression levels of miR-miR-150-5p and TP53 in colon adenocarcinoma and adjacent non-cancerous tissue samples, or in human colon adenocarcinoma cell lines. MTT assay was used to determine proliferation and apoptosis in cell lines. Furthermore, we used Western blot to determine levels of cell cycle regulators with anti-miR-150-5p or apoptosis with overexpression of TP53. Our results show that expression levels of miR-150-5p were significantly elevated in clinical specimens from cancer patients. We further showed that inhibition of miR-150-5p increased TP53, and in turn, suppression of proliferation of colon adenocarcinoma. Moreover, inhibition of miR-150-5p or overexpression of TP53 caused cell arrest or apoptosis in colon adenocarcinoma. Our results support that miR-150-5p-TP53 pathway plays an important role in regulation of proliferation, cell arrest, and apoptosis in colon cancer, and could be an attractive target for therapy.

Achieving the activation of drugs within cellular systems may provide targeted therapies. Here we construct a tumour-selective cascade activatable self-detained system (TCASS) and incorporate imaging probes and therapeutics. We show in different mouse models that the TCASS system accumulates in solid tumours. The molecules show enhanced accumulation in tumour regions via the effect of recognition induced self-assembly. Analysis of the molecular penetration in tumour tissue shows that in vivo self-assembly increases the penetration capability compared to typical soft or hard nanomaterials. Importantly, the in vivo self-assembled molecules exhibit a comparable clearance pathway to that of small molecules, which are excreted from organs of the reticuloendothelial system (liver and kidney), while are relatively slowly eliminated from tumour tissues. Finally, this system, combined with the NIR probe, shows high specificity and sensitivity for detecting bladder cancer in isolated intact patient bladders. The activation of drugs within cellular systems may provide targeted therapies for cancer. Here, the authors make a drug delivery system that is activated within the cell and exploits XIAP expression to cleave a linker region, resulting in the self-assembly of the system and drug release within cancer cells.

Among the many immunosuppressive cells in the tumor microenvironment, tumor-associated-macrophages (TAMs) are well known to contribute to tumor development. TAMs can be conditioned (polarized) to transition between classical M1-like macrophages, or alternatively to M2-like macrophages. Both are regulated by signaling molecules in the microenvironment. M1-like TAMs can secrete classic inflammatory cytokines that kill tumors by promoting tumor cell necrosis and immune cell infiltration into the tumor microenvironment. In contrast, M2-like TAMs exhibit powerful tumor-promoting functions, including degradation of tumor extracellular matrix, destruction of basement membrane, promotion of angiogenesis, and recruitment of immunosuppressor cells, all of which further promote tumor progression and distal metastasis. Therefore, remodeling the tumor microenvironment by reversing the TAM phenotype will be favorable for tumor therapy, especially immunotherapy. PLGA nanoparticles encapsulating baicalin and melanoma antigen Hgp peptide fragment 25-33 were fabricated using the ultrasonic double-emulsion technique. The nanoparticles were further loaded with CpG fragments and used conjugated M2pep and α-pep peptides on their surfaces to produce novel nano-complexes. The capability to target M2-like TAMs and anti-tumor immunotherapy effects of nano-complexes were evaluated by flow cytometry and confocal microscopy . We also investigated the survival and histopathology of murine melanoma models administrated with different nanocomplexes. Improvements in the tumor microenvironment for immune attack of melanoma-bearing mice were also assessed. The nano-complexes were effectively ingested by M2-like TAMs and , and the acidic lysosomal environment triggered the disintegration of polydopamine from the nanoparticle surface, which resulted in the release of the payloads. The released CpG played an important role in transforming the M2-like TAMs into the M1-like phenotype that further secreted inflammatory cytokines. The reversal of TAM released cytokines and gradually suppressed tumor angiogenesis, permitting the remodeling of the tumor microenvironment. Moreover, the activated TAMs also presented antigen to T cells, which further stimulated the antitumor immune response that inhibited tumor metastasis. Activated T cells released cytokines, which stimulated NK cell infiltration and directly resulted in killing tumor cells. The baicalin released by M1-like TAMs also killed tumor cells. The nano-complexes facilitated baicalin, antigen, and immunostimulant delivery to M2-like TAMs, which polarized and reversed the M2-like TAM phenotype and remodeled the tumor microenvironment to allow killing of tumor cells.