Persistence and Stability for a Generalized Leslie-Gower Model with Stage Structure and Dispersal

A generalized version of the Leslie-Gower predator-prey model that incorporates the prey structure and predator dispersal in two-patch environments is introduced. The focus is on the study of the boundedness of solution, permanence, and extinction of the model. Sufficient conditions for global asymptotic stability of the positive equilibrium are derived by constructing a Lyapunov functional. Numerical simulations are also presented to illustrate our main results

Diaqua­(5-methyl­pyrazine-2-carboxyl­ato-κ2 N 1,O)iron(II)

In the neutral title complex, [Fe(C6H5N2O2)2(H2O)2], the coordination geometry aound the FeII atom, which lies on an inversion centre, is distorted octa­hedral comprising two N atoms and two O atoms from two 5-methyl­pyrazine-2-carboxyl­ate ligands, and two water mol­ecules. The crystal structure is stabilized by a network of O—H⋯O hydrogen bonds, resulting in a two-dimensional supra­molecular structure

A Lattice Study of (Dˉ1D∗)±(\bar{D}_1 D^{*})^\pm Near-threshold Scattering

In this exploratory lattice study, low-energy near threshold scattering of the $(\bar{D}_1 D^{*})^\pm$ meson system is analyzed using lattice QCD with $N_f=2$ twisted mass fermion configurations. Both s-wave ($J^P=0^-$) and p-wave ($J^P=1^+$) channels are investigated. It is found that the interaction between the two charmed mesons is attractive near the threshold in both channels. This calculation provides some hints in the searching of resonances or bound states around the threshold of $(\bar{D}_1 D^{*})^\pm$ system.Comment: 20 pages, 15 figures, matches the version on PR

3,5-Bis(4-methoxy­phen­yl)-1H-1,2,4-triazole monohydrate

In the title compound, C16H15N3O2·H2O, the two benzene rings and the triazole ring lie almost in the same plane, the triazole ring forming dihedral angles of 5.07 (9) and 5.80 (8)° with the benzene rings. In the crystal, there are three relatively strong inter­molecular O—H⋯N and N—H⋯O hydrogen bonds, which lead to the formation of a one-dimensional double chain running parallel to the a axis. Weak π—π inter­actions between the benzene rings of neighboring chains with a centroid–centroid distance of 3.893 (4) Å result in the formation of layers parallel to the ac plane

3-O-Caffeoylquinic acid in Periploca forrestii Schltr extract ameliorates collagen-induced arthritis by inducing IL17/IL23 cells in rats

Purpose: To study the therapeutic effect of 3-O-caffeoylquinic acid (3-O-CQA) from Periploca forrestii extract (PFE) on collagen-mediated arthritis (CIA) in rats, as well as the potential underlying mechanism of action. Methods: PFE and 3-O-CQA were successively and intragastrically administered to CIA rats. Paw swelling, arthritic scores and H & E staining were used to evaluate the therapeutic effect of 3-O-CQA. Moreover, to determine the effects of PFE and 3-O-CQA on fibroblast-resembling synoviocytes obtained from arthritic subjects (RAFLS), the viability of RAFLS cultured in vitro was measured with MMT, while apoptotic lesions were analyzed by flow cytometry. The levels of IL-6 in CIA and RAFLS were determined by enzyme-linked immunosorbent assay (ELISA), while quantitative reverse transcriptionpolymerase chain reaction (qRT-PCR) and immunoblotting were used to assess their mRNA and polypeptide levels, respectively. Results: PFE in 3-O-CQA ameliorated swelling and reduced arthritic scores in CIA rat model, and also decreased cytokine levels (p < 0.05). By decreasing mRNA and protein expressions, 3-O-CQA repressed the phosphorylation of STAT3 and JAK2 as well as the protein levels of IL-23 and RORγt (p < 0.05). Conclusion: The results of this study show that CIA and RAFLS are ameliorated in rats by 3-O-CQA in PFE through regulation of IL17/ IL23 and Th17 cells. Thus, 3-O-CQA affords a therapeutic strategy for the management of collagen-induced arthritis. Keywords: Arthriti; Periploca forrestii Schltr extract; 3-O-Caffeoylquinic acid; Interleukin (IL)-17; IL-23; Th17 cell

Two Photon Decays of ηc\eta_c from Lattice QCD

We present an exploratory lattice study for the two-photon decay of $\eta_c$ using $N_f=2$ twisted mass lattice QCD gauge configurations generated by the European Twisted Mass Collaboration. Two different lattice spacings of $a=0.067$fm and $a=0.085$fm are used in the study, both of which are of physical size of 2$fm$. The decay widths are found to be $1.025(5)$KeV for the coarser lattice and $1.062(5)$KeV for the finer lattice respectively where the errors are purely statistical. A naive extrapolation towards the continuum limit yields $\Gamma\simeq 1.122(14)$KeV which is smaller than the previous quenched result and most of the current experimental results. Possible reasons are discussed.Comment: 13 pages, 7 figures; matches the published versio

Low-energy Scattering of (D∗Dˉ∗)±(D^{*}\bar{D}^{*})^\pm System and the Resonance-like Structure Zc(4025)Z_c(4025)

In this paper, low-energy scattering of the $(D^{*}\bar{D}^{*})^\pm$ meson system is studied within L\"uscher's finite-size formalism using $N_{f}=2$ twisted mass gauge field configurations. With three different pion mass values, the $s$-wave threshold scattering parameters, namely the scattering length $a_0$ and the effective range $r_0$, are extracted in $J^P=1^+$ channel. Our results indicate that, in this particular channel, the interaction between the two vector charmed mesons is weakly repulsive in nature hence do not support the possibility of a shallow bound state for the two mesons, at least for the pion mass values being studied. This study provides some useful information on the nature of the newly discovered resonance-like structure $Z_c(4025)$ observed in various experiments.Comment: 11 pages, 6 figures. arXiv admin note: substantial text overlap with arXiv:1403.131

Extracellular Matrix Protein Tenascin C Increases Phagocytosis Mediated by CD47 Loss of Function in Glioblastoma.

Glioblastomas (GBM) are highly infiltrated by myeloid-derived innate immune cells that contribute to the immunosuppressive nature of the brain tumor microenvironment (TME). CD47 has been shown to mediate immune evasion, as the CD47-SIRPα axis prevents phagocytosis of tumor cells by macrophages and other myeloid cells. In this study, we established CD47 homozygous deletion (CD47-/-) in human and mouse GBM cells and investigated the impact of eliminating the "don't eat me" signal on tumor growth and tumor-TME interactions. CD47 knockout (KO) did not significantly alter tumor cell proliferation in vitro but significantly increased phagocytosis of tumor cells by macrophages in cocultures. Compared with CD47 wild-type xenografts, orthotopic xenografts derived from CD47-/- tumor cells grew significantly slower with enhanced tumor cell phagocytosis and increased recruitment of M2-like tumor-associated microglia/macrophages (TAM). CD47 KO increased tumor-associated extracellular matrix protein tenascin C (TNC) in xenografts, which was further examined in vitro. CD47 loss of function upregulated TNC expression in tumor cells via a Notch pathway-mediated mechanism. Depletion of TNC in tumor cells enhanced the growth of CD47-/- xenografts in vivo and decreased the number of TAM. TNC knockdown also inhibited phagocytosis of CD47-/- tumor cells in cocultures. Furthermore, TNC stimulated release of proinflammatory factors including TNFα via a Toll-like receptor 4 and STAT3-dependent mechanism in human macrophage cells. These results reveal a vital role for TNC in immunomodulation in brain tumor biology and demonstrate the prominence of the TME extracellular matrix in affecting the antitumor function of brain innate immune cells. SIGNIFICANCE: These findings link TNC to CD47-driven phagocytosis and demonstrate that TNC affects the antitumor function of brain TAM, facilitating the development of novel innate immune system-based therapies for brain tumors

Tim-3 Negatively Regulates IL-12 Expression by Monocytes in HCV Infection

T cell immunoglobulin and mucin domain-containing protein 3 (Tim-3) is a newly identified negative immunomodulator that is up-regulated on dysfunctional T cells during viral infections. The expression and function of Tim-3 on human innate immune responses during HCV infection, however, remains poorly characterized. In this study, we report that Tim-3 is constitutively expressed on human resting CD14+ monocyte/macrophages (M/MØ) and functions as a cap to block IL-12, a key pro-inflammatory cytokine linking innate and adaptive immune responses. Tim-3 expression is significantly reduced and IL-12 expression increased upon stimulation with Toll-like receptor 4 (TLR4) ligand - lipopolysaccharide (LPS) and TLR7/8 ligand - R848. Notably, Tim-3 is over-expressed on un-stimulated as well as TLR-stimulated M/MØ, which is inversely associated with the diminished IL-12 expression in chronically HCV-infected individuals when compared to healthy subjects. Up-regulation of Tim-3 and inhibition of IL-12 are also observed in M/MØ incubated with HCV-expressing hepatocytes, as well as in primary M/MØ or monocytic THP-1 cells incubated with HCV core protein, an effect that mimics the function of complement C1q and is reversible by blocking the HCV core/gC1qR interaction. Importantly, blockade of Tim-3 signaling significantly rescues HCV-mediated inhibition of IL-12, which is primarily expressed by Tim-3 negative M/MØ. Tim-3 blockade reduces HCV core-mediated expression of the negative immunoregulators PD-1 and SOCS-1 and increases STAT-1 phosphorylation. Conversely, blocking PD-1 or silencing SOCS-1 gene expression also decreases Tim-3 expression and enhances IL-12 secretion and STAT-1 phosphorylation. These findings suggest that Tim-3 plays a crucial role in negative regulation of innate immune responses, through crosstalk with PD-1 and SOCS-1 and limiting STAT-1 phosphorylation, and may be a novel target for immunotherapy to HCV infection