Incommensurate itinerant antiferromagnetic excitations and spin resonance in the FeTe0.6_{0.6}Se0.4_{0.4} superconductor

We report on inelastic neutron scattering measurements that find incommensurate itinerant like magnetic excitations in the normal state of superconducting FeTe$_{0.6}$Se$_{0.4}$ (\Tc=14K) at wave-vector $\mathbf{Q}_{inc}=(1/2\pm\epsilon,1/2\mp\epsilon)$ with $\epsilon$=0.09(1). In the superconducting state only the lower energy part of the spectrum shows significant changes by the formation of a gap and a magnetic resonance that follows the dispersion of the normal state excitations. We use a four band model to describe the Fermi surface topology of iron-based superconductors with the extended $s(\pm)$ symmetry and find that it qualitatively captures the salient features of these data.Comment: 7 pages and 5 figure

Molecular cloning and characterization of a new peroxidase gene (OvRCI) from Orychophragmus violaceus

A new peroxidase gene from Orychophragmus violaceus was cloned. The full-length cDNA of O.violaceus peroxidase gene (OvRCI, GenBank. Acc. No. AY428037) was 1220 bp and contained an 1128 bp open reading frame encoding a protein of 375 amino acids. Homology analysis and molecularmodeling revealed that OvRCI strongly resembled other peroxidase genes. Quantitative real-time PCR analysis revealed that it was a constitutively salt-inducible gene and its transcript level was most abundant after 24 h treatment with 200 mmol.L-1 sodium chloride. Our studies suggested that OvRCI was a new member of the family of recently cloned peroxidase genes

LNK suppresses interferon signaling in melanoma.

LNK (SH2B3) is a key negative regulator of JAK-STAT signaling which has been extensively studied in malignant hematopoietic diseases. We found that LNK is significantly elevated in cutaneous melanoma; this elevation is correlated with hyperactive signaling of the RAS-RAF-MEK pathway. Elevated LNK enhances cell growth and survival in adverse conditions. Forced expression of LNK inhibits signaling by interferon-STAT1 and suppresses interferon (IFN) induced cell cycle arrest and cell apoptosis. In contrast, silencing LNK expression by either shRNA or CRISPR-Cas9 potentiates the killing effect of IFN. The IFN-LNK signaling is tightly regulated by a negative feedback mechanism; melanoma cells exposed to IFN upregulate expression of LNK to prevent overactivation of this signaling pathway. Our study reveals an unappreciated function of LNK in melanoma and highlights the critical role of the IFN-STAT1-LNK signaling axis in this potentially devastating disease. LNK may be further explored as a potential therapeutic target for melanoma immunotherapy

Effects of NaCl treatment on the antioxidant enzymes of oilseed rape (Brassica napus L.) seedlings

The effects of NaCl treatment on the activity of antioxidant enzymes in leaves of oilseed rape seedlings (Brassica napus L.) were studied. The results showed that the relative water content from leaves of oilseed rape seedlings was gradually decreased and the electronic conductivity was increased during 0 - 24 h under 200 mmol.l-1 NaCl treatments. The activity of peroxidase (POD), superoxide dismutase (SOD) and catalase (CAT) was gradually increased during 0 - 24 h under 200 mmol.l-1 NaCl stress. After 24 h, the activities of these antioxidases were maximum and subsequently decreased. Quantitative realtime PCR analysis revealed that they were salt-inducible genes and their transcript levels were gradually increased during 0 - 24 h and most abundant after 24 h treatment with 200 mmol.l-1 sodium chloride. Therefore, these results from above indicated that the expressions of POD, SOD and CAT genes were induced by NaCl; the activities of POD, SOD and CAT were increased, which enhanced the tolerance of oilseed oilseed rape plants against NaCl stress

A proposed reaction channel for the synthesis of the superheavy nucleus Z = 109

We apply a statistical-evaporation model (HIVAP) to calculate the cross sections of superheavy elements, mainly about actinide targets and compare with some available experimental data. A reaction channel $^{30}$Si + $^{243}$Am is proposed for the synthesis of the element Z = 109 and the cross section is estimated.Comment: 4 pages, 2 figures, 2 tables; two typos are corrected in Ref. [12] and [19

Dynamics of Davydov Ansatze

Following the Dirac-Frenkel time-dependent variational principle, dynamics of a one-dimensional Holstein polaron is probed by employing the Davydov D2 Ansatz with two sets of variational parameters, one for each constituting particle in the exciton-phonon system, and a simplified variant of the Davydov D1 Ansatz, also known as the $\tilde{D}$ Ansatz, with an additional set of phonon displacement parameters. A close examination of variational outputs from the two trial states reveals fine details of the polaron structure and intricacies of dynamic exciton-phonon interactions. Superradiance coherence sizes, speeds of exciton-induced phonon wave packets, linear optical absorption, and polaron energy compositions are also included in the study.Comment: 14 pages and 11 figue

Total Reaction Cross Section in an Isospin-Dependent Quantum Molecular Dynamics (IDQMD) Model

The isospin-dependent quantum molecular dynamics (IDQMD) model is used to study the total reaction cross section $\sigma_R$. The energy-dependent Pauli volumes of neutrons and protons have been discussed and introduced into the IDQMD calculation to replace the widely used energy-independent Pauli volumes. The modified IDQMD calculation can reproduce the experimental $\sigma_R$ well for both stable and exotic nuclei induced reactions. Comparisons of the calculated $\sigma_R$ induced by $^{11}Li$ with different initial density distributions have been performed. It is shown that the calculation by using the experimentally deduced density distribution with a long tail can fit the experimental excitation function better than that by using the Skyrme-Hartree-Fock calculated density without long tails. It is also found that $\sigma_R$ at high energy is sensitive to the long tail of density distribution.Comment: 4 page, 4 fig

Escherichia coli adhesion protein FimH exacerbates colitis via CD11b+CD103- dendritic cell activation

IntroductionImmune stimulators are used to improve vaccine efficiency; however, they are accompanied by various side effects. In previous studies, we reported that the Escherichia coli adhesion protein, FimH, induces immune activity; however, we did not examine any side effects in colon inflammation.MethodsFimH was administered orally or intraperitoneally (i.p.) to mice with dextran sulfate sodium (DSS)-induced colitis, and changes in symptoms were observed. Immune cells infiltrated into the colon after the induction of colon inflammation were analyzed using a flow cytometer. Changes in Th1 and Th17 cells that induce colitis were analyzed. Further, mesenteric lymph node (mLN) dendritic cells (DCs) activated by FimH were identified and isolated to examine their ability to induce T-cell immunity.ResultsFimH oral and i.p. administration in C57BL/6 mice did not induce inflammation in the colon; however, DSS-induced colitis was exacerbated by oral and i.p. FimH administration. FimH treatment increased immune cell infiltration in the colon compared to that in DSS colitis. Th1 and Th17 cells, which are directly related to colitis, were increased in the colon by FimH; however, FimH did not directly affect the differentiation of these T cells. FimH upregulated the CD11b+CD103- DC activity in the mLNs, which produced the signature cytokines required for Th1 and Th17. In addition, isolated CD11b+CD103- DCs, after stimulation with FimH, directly induced Th1 and Th17 differentiation in a co-culture of CD4 T cells.ConclusionThis study demonstrated the side effects of FimH and indicated that the use of FimH can aggravate the disease in patients with colitis

Ack1 Mediated AKT/PKB Tyrosine 176 Phosphorylation Regulates Its Activation

The AKT/PKB kinase is a key signaling component of one of the most frequently activated pathways in cancer and is a major target of cancer drug development. Most studies have focused on its activation by Receptor Tyrosine Kinase (RTK) mediated Phosphatidylinositol-3-OH kinase (PI3K) activation or loss of Phosphatase and Tensin homolog (PTEN). We have uncovered that growth factors binding to RTKs lead to activation of a non-receptor tyrosine kinase, Ack1 (also known as ACK or TNK2), which directly phosphorylates AKT at an evolutionarily conserved tyrosine 176 in the kinase domain. Tyr176-phosphorylated AKT localizes to the plasma membrane and promotes Thr308/Ser473-phosphorylation leading to AKT activation. Mice expressing activated Ack1 specifically in the prostate exhibit AKT Tyr176-phosphorylation and develop murine prostatic intraepithelial neoplasia (mPINs). Further, expression levels of Tyr176-phosphorylated-AKT and Tyr284-phosphorylated-Ack1 were positively correlated with the severity of disease progression, and inversely correlated with the survival of breast cancer patients. Thus, RTK/Ack1/AKT pathway provides a novel target for drug discovery