Signature of Pseudo Nambu-Goldstone Higgs boson in its Decay

If the Higgs boson is a pseudo Nambu-Goldstone boson (PNGB), the $hZ\gamma$ contact interaction induced by the $\mathcal{O}(p^4)$ invariants of the non-linear sigma model is free from its nonlinearity effects. The process $h\rightarrow Z\gamma$ can be used to eliminate the universal effects of heavy particles, which can fake the nonlinearity effects of the PNGB Higgs boson in the process $h\rightarrow V^*V$ ($V=W^\pm$,\ $Z$). We demonstrate that the ratio of the signal strength of $h\rightarrow Z\gamma$ and $h\rightarrow V^*V$ is good to distinguish the signature of the PNGB Higgs boson from Higgs coupling deviations

ZMCintegral-v5.1: Support for Multi-function Integrations on GPUs

In this new version of ZMCintegral, we have added the functionality of multi-function integrations, i.e. the ability to integrate more than $10^{3}$ different functions on GPUs. The Python API remains the similar as the previous versions. For integrands less than 5 dimensions, it usually takes less than 10 minutes to finish the evaluation of $10^{3}$ integrations on one Tesla v100 card. The performance scales linearly with the increasing of the GPUs.Comment: 5pages, 1figur

Ethyl 2-methyl-4-phenyl­pyrido[1,2-a]benzimidazole-3-carboxyl­ate

The title compound, C21H18N2O2, was synthesized using a novel tandem annulation reaction between (1H-benzimidazol-2-yl)(phen­yl)methanone and (E)-ethyl 4-bromo­but-2-enoate under mild conditions. The dihedral angles between the mean planes of the five-membered imidazole ring and the pyridine, benzene and phenyl rings are 0.45 (6), 1.69 (1) and 70.96 (8)°, respectively. In the crystal, mol­ecules are linked through inter­molecular C—H⋯N hydrogen bonds

Bis{2-[bis­(3,5-dimethyl-1H-pyrazol-1-yl-κN 2)meth­yl]pyridine-κN}cobalt(II) dinitrate

The central CoII ion in the title complex, [Co(C16H19N5)2](NO3)2, is located on a twofold rotation axis and has a slightly distorted octa­hedral coordination sphere. It is bonded to six N atoms from two 2-[bis­(3,5-dimethyl-1H-pyrazol-1-yl)meth­yl]pyridine ligands. In the crystal, mol­ecules are linked by weak C—H⋯O inter­actions

Overexpression of long non-coding RNA NORAD promotes invasion and migration in malignant melanoma via regulating the MIR-205-EGLN2 pathway.

Growing evidence suggests that long non-coding RNAs NORAD and miR-205 play a significant role in regulating cancer progression and metastasis. In this study, high expression of NORAD was firstly observed in melanoma tissues and human malignant melanoma cell lines, our aim was to study the interaction of them in the process of invasion and migration of malignant melanoma cells. NORAD, miR-205, and EGLN2 mRNA level in MM cells was detected by qRT-PCR. In situ hybridization (ISH) was performed to detect NORAD expression in MM tissues specimens. Effects of NORAD and miR-205 on Prolyl hydroxylase 2 (EGLN2) expression was explored by western blot in MM cells line. Dual-luciferase reporter assay was performed to verify the interaction relationship between NORAD and miR-205, as well as, miR-205 and EGLN2. Transwell assay was conducted to explore the effects of NORAD and miR-205 in vitro. Xenografts in nude mice experiment were used to confirm the role of NORAD and miR-205 in vivo. In vitro, NORAD knockdown significantly inhibited migration and invasion of malignant melanoma cells and elevated the expression of miR-205, there was an interaction between miR-205 and NORAD in the RNA-induced silencing complex. Upregulation of miR-205 induced significant inhibition of migratory and invasive ability compared with the scrambled control. However, downregulating NORAD largely reversed this effect. Furthermore, the regulatory effects of miR-205 on EGLN2 levels and the induction of endoplasmic reticulum stress were reversed by NORAD. In vivo, deletion of miR-205 induced tumor growth in nude mice. NORAD may play critical roles in tumorigenesis and progression of malignant melanoma by regulating of the miR-205-EGLN2 pathway, and may serve as a new therapeutic target