Quantum molecular dynamic simulations of warm dense carbon monoxide

Using quantum molecular dynamic simulations, we have studied the thermophysical properties of warm dense carbon monoxide under extreme conditions. The principal Hugoniot, which is derived from the equation of state, shows excellent agreement with available experimental data up to 67 GPa. The chemical decomposition of carbon monoxide has been predicted at 8 GPa by means of pair correlation function. Based on Kubo-Greenwood formula, the dc electrical conductivity and the optical reflectivity are determined, and the nonmetal-metal transition for shock compressed carbon monoxide is observed around 43 GPa

5-(Pyridin-4-yl)isophthalic acid

In the title compound, C13H9NO4, the two carb­oxy­lic groups and the benzene ring are approximately co-planar with a maximum atomic deviation 0.175 (4) Å, while the pyridine ring is oriented at a dihedral angle of 31.07 (18)° with respect to the benzene ring. In the crystal, mol­ecules are linked by O—H⋯O, O—H⋯N and weak C—H⋯O hydrogen bonds, forming a three-dimensional supra­molecular framework

Intrinsic topological superconductivity with exactly flat surface bands in the quasi-one-dimensional A2_2Cr3_3As3_3 (A=Na, K, Rb, Cs) superconductors

A spin-U(1)-symmetry protected momentum-dependent integer-$Z$-valued topological invariant is proposed to time-reversal-invariant (TRI) superconductivity (SC) whose nonzero value will lead to exactly flat surface band(s). The theory is applied to the weakly spin-orbit coupled quasi-1D A$_2$Cr$_3$As$_3$ (A=Na, K, Rb, Cs) superconductors family with highest $T_c$ up to 8.6 K with $p_z$-wave pairing in the $S_z=0$ channel. It's found that up to the leading atomic spin-orbit-coupling (SOC), the whole (001) surface Brillouin zone is covered with exactly-flat surface bands, with some regime hosting three flat bands and the remaining part hosting two. Such exactly-flat surface bands will lead to very sharp zero-bias conductance peak in the scanning tunneling microscopic spectrum. When a tiny subleading spin-flipping SOC is considered, the surface bands will only be slightly split. The application of this theory can be generalized to other unconventional superconductors with weak SOC, particularly to those with mirror-reflection symmetry.Comment: 4.5pages, 4 figures plus Appendi

Role of hepatitis B surface antigen in the development of hepatocellular carcinoma: regulation of lymphoid enhancer-binding factor 1

<p>Abstract</p> <p>Background</p> <p>There are around 350 million of hepatitis B surface antigen (HBsAg) carriers worldwide, and among them, high risk of developing hepatocellular carcinoma (HCC) has been identified by epidemiological studies. To date, the molecular role of HBsAg in HCC development has not been fully studied. We have previously reported that in cell cultures, HBsAg up-regulated the expression of lymphoid enhancer-binding factor 1 (LEF-1), a key component of the <it>Wnt </it>pathway. In this study we aimed to study this effect of HBsAg on LEF-1 in the development of HCC.</p> <p>Methods</p> <p>Expression of HBsAg, LEF-1 and its downstream effector genes were compared among 30 HCCs, their peritumor tissue counterparts and 9 normal control liver tissues by quantitative real-time PCR. In addition, immunohistochemical staining studies on HBsAg and LEF-1 expression were conducted among these samples.</p> <p>Results</p> <p>The expression of LEF-1 was compared between 13 HBsAg positive HCC tissues and 17 HBsAg negative HCC tissues. Simultaneous detection of LEF-1 and HBsAg was observed in HBsAg positive HCC tissues and, additionally, the simultaneous detection of HBsAg and LEF-1 was more pronounced in peritumor tissues, compared to that in the tumor tissues. The distribution of cellular LEF-1 in peritumor tissues was predominantly in the cytoplasm; while LEF-1 in the tumor tissues was located either exclusively in the nucleus or both in the nucleus and cytoplasm. By real-time PCR, the expression levels of LEF-1 downstream effector genes <it>cyclin D1 </it>and <it>c-myc </it>were higher in peritumor cells compared to that of the tumor cells. However, a 38 kDa truncated isoform of LEF-1, rather than the 55 kDa wild-type LEF-1, was significantly elevated in the HBsAg positive tumor cells.</p> <p>Conclusion</p> <p>Data indicate that deregulation of the <it>Wnt </it>pathway by HBsAg occurred in HBV-associated HCCs, but was more pronounced in the peritumor cells. It is speculated that HBsAg could stimulate proliferation and functional modification of hepatocytes via LEF-1 through the <it>Wnt </it>pathway at the pre-malignant stage.</p

NOK/STYK1 interacts with GSK-3β and mediates Ser9 phosphorylation through activated Akt

AbstractNOK (also known as STYK1) has been identified as an oncogene. However, its biochemical and biological activities as a molecular regulator are poorly defined. In the present study, we report that NOK overexpression led to enhanced phosphorylation of GSK-3β at its Ser9 residue via Akt phosphorylation at Thr308. NOK could make complexes with both Akt and GSK-3β. Moreover, the expression levels of NOK, p-Akt(Thr308) and p-GSK-3β(Ser9) were positively correlated in cancerous and non-cancerous breast cell lines. Thus, our data identified a novel functional molecular complex formed by NOK, Akt and GSK-3β that may relay a NOK-directed tumourigenic cascade.Structured summary of protein interactionsGSK3B physically interacts with NOK and Akt by anti tag coimmunoprecipitation (View interaction).GSK3B physically interacts with NOK by anti tag coimmunoprecipitation (View interaction)