1,5-Diphenyl­carbonohydrazide N,N-di­methyl­formamide

In the title compound, C13H14N4O·C3H7NO, a 1,5-phenyl­carbonohydrazide mol­ecule cocrystallizes with an N,N-dimethyl­formamide mol­ecule. In the 1,5-phenyl­carbonohydrazide mol­ecule, the two phenyl rings are twisted by an angle of 45.8 (5)°. Inter­molecular N—H⋯O hydrogen bonds and weak inter­molecular C—H⋯O inter­actions contribute to a supra­molecular two-dimensional network in the (101) plane

Biphenyl-2,2′,4,4′-tetra­carb­oxy­lic acid monohydrate

In the title compound, C16H10O8·H2O, the dihedral angle between the two benzene rings is 71.63 (5)°. In the crystal structure, pairs of inversion-related mol­ecules are stacked [mean inter­planar spacing = 3.5195 (18) Å], and O—H⋯O and C—H⋯O hydrogen bonds create a three-dimensional network

ISG15 inhibits IFN- a -Resistant liver cancer cell growth

Hepatocellular carcinoma (HCC) is one of the most prevalent tumors worldwide. Interferon-a (IFN-a) has been widely used in the treatment of HCC, but patients eventually develop resistance. ISG15 ubiquitin-like modifier (ISG15) is a ubiquitin-like protein transcriptionally regulated by IFN-a which shows antivirus and antitumor activities. However, the exact role of ISG15 is unknown. In the present study, we showed that IFN-a significantly induced ISG15 expression but failed to induce HepG2 cell apoptosis, whereas transient overexpression of ISG15 dramatically increased HepG2 cell apoptosis. ISG15 overexpression increased overall protein ubiquitination, which was not observed in cells with IFN-a-induced ISG15 expression, suggesting that IFN-a treatment not only induced the expression of ISG15 but also inhibited ISG15-mediated ubiquitination. The tumor suppressor p53 and p21 proteins are the key regulators of cell survival and death in response to stress signals such as DNA damage. We showed that p53 or p21 is only up regulated in HepG2 cells ectopically expressing ISG15, but not in the presence of IFN-a-induced ISG15. Our results suggest that ISG15 overexpression could be developed into a powerful gene-therapeutic tool for treating IFN-a-resistant HCC. © 2013 Xin-xing Wan et al

Aqua­[N-phenyl-2-(quinolin-8-yl­oxy)acetamide]dinitratozinc(II)

In the title complex, [Zn(NO3)2(C17H14N2O2)(H2O)], the six-coordinated Zn atom is in a distorted octa­hedral geometry, the donor centers being two O atoms and one N atom from the tridentate organic ligand, a water O atom and two O atoms from two monodentate nitrate ions. In the crystal, O—H⋯O hydrogen bonds between the coordinated water mol­ecules and nitrate O atoms and N—H⋯O hydrogen bonds between the main ligand and nitrate O atoms consolidate the three-dimensional network

JPJ^P Assignments of Λc+\Lambda_c^+ Baryons

The "good" diquark is employed to study $\Lambda_c^{+}$ baryons within a mass loaded flux tube model. The study indicates that all $\Lambda_c^{+}$ baryons candidates in the 2008 review by the Particle Data Group (PDG) are well described in the mass loaded flux tube model. The quantum numbers $J^P$ of these $\Lambda_c^{+}$ candidates are assigned. If $\Lambda_c(2765)^{+}$ is an orbitally excited $\Lambda^+_c$, it is likely the $J^P={3\over 2}^+$ one. If $\Lambda_c(2765)^+$ is an orbitally excited $\Sigma_c$, there ought to be another $J^P={3\over 2}^+$ $\Lambda^+_c$ with mass $\approx 2770$ MeV. In the model, there exists no $J^P={1\over 2}^+$ $\Lambda_c(\approx 2700)^+$ predicted in existing literature. $\Lambda_c(2940)^{+}$ is very possible the orbitally excited baryon with $J^P={5\over 2}^-$.Comment: 4 pages, 3 tables, RevTex, Two typos correcte

Cigarette Smoke Extract Stimulates Rat Pulmonary Artery Smooth Muscle Cell Proliferation via PKC-PDGFB Signaling

Accumulating evidence suggests a direct role for cigarette smoke in pulmonary vascular remodeling, which contributes to the development of pulmonary hypertension. However, the molecular mechanisms underlying this process remain poorly understood. Platelet-derived growth factor (PDGF) is a potential mitogen and chemoattractant implicated in several biological processes, including cell survival, proliferation, and migration. In this study, we investigated the effect of cigarette smoke extract (CSE) on cell proliferation of rat pulmonary artery smooth muscle cells (rPASMCs). We found that stimulation of rPASMCs with CSE significantly increased cell proliferation and promoted cell cycle progression from G1 phase to the S and G2 phases. CSE treatment also significantly upregulated the mRNA and protein levels of PDGFB and PDGFRβ. Our study also revealed that Rottlerin, an inhibitor of PKCδ signaling, prevented CSE-induced cell proliferation, attenuated the increase of S and G2 phase populations induced by CSE treatment, and downregulated PDGFB and PDGFRβ mRNA and protein levels in rPASMCs exposed to CSE. Collectively, our data demonstrated that CSE-induced cell proliferation of rPASMCs involved upregulation of the PKCδ-PDGFB pathway

Analyzing Gene Expression Profile in K562 Cells Exposed to Sodium Valproate Using Microarray Combined with the Connectivity Map Database

To explore the mechanism underlying antileukaemia effect of sodium valproate, the growth and survival of the K562 cell line were investigated. Global profiles of gene expression in K562 cells exposed to sodium valproate were assessed and validated. The differentially expressed genes identified were further used to query the connectivity map database to retrieve a ranked list of compounds that act on the same intracellular targets as sodium valproate. A significant increase in cell apoptosis and a change in gene expression profile were observed in valproate-exposed K562 cells. The significant enrichment analysis of gene ontology terms for the differentially expressed genes showed that these genes were involved in many important biological processes. Eight differentially expressed genes involved in apoptosis were verified by quantitative real-time PCR. The connectivity map analysis showed gene expression profile in K562 cells exposed to sodium valproate was most similar to that of HDACi and PI3K inhibitors, suggesting that sodium valproate might exert antileukaemic action by inhibiting HDAC as well as inhibiting PI3K pathway. In conclusion, our data might provide clues to elucidate the molecular and therapeutic potential of VPA in leukaemia treatment, and the connectivity map is a useful tool for exploring the molecular mechanism of drug action

Bis[N-benzyl-2-(quinolin-8-yl­oxy)acetamide]dichloridocopper(II) acetonitrile solvate monohydrate

In the title complex, [CuCl2(C18H16N2O2)2]·CH3CN·H2O, the six-coordinated Cu atom is in a distorted octa­hedral geometry with the donor centers of two O atoms and two N atom from two bidentate ligands, and two chloride ions. In the crystal, pairs of inter­molecular N—H⋯ Cl hydrogen bonds form centrosymmetric dimers and inter­molecular O—H⋯ O hydrogen bonds between the ligand and the uncoordinated water mol­ecules link the dimers into chains parallel to the c axis

Downregulation of CD147 expression alters cytoskeleton architecture and inhibits gelatinase production and SAPK pathway in human hepatocellular carcinoma cells

<p>Abstract</p> <p>Background</p> <p>CD147 plays a critical role in the invasive and metastatic activity of hepatocellular carcinoma (HCC) cells by stimulating the surrounding fibroblasts to express matrix metalloproteinases (MMPs). Tumor cells adhesion to extracellular matrix (ECM) proteins is the first step to the tumor metastasis. MMPs degrade the ECM to promote tumor metastasis. The aim of this study is to investigate the effects of small interfering RNA (siRNA) against CD147 (si-CD147) on hepatocellular carcinoma cells' (SMMC-7721) architecture and functions.</p> <p>Methods</p> <p>Flow cytometry and western blot assays were employed to detect the transfection efficiency of si-CD147. Confocal microscopy was used to determine the effects of si-CD147 on SMMC-7721 cells' cytoskeleton. Invasion assay, gelatin zymography and cell adhesion assay were employed to investigate the effects of si-CD147 on SMMC-7721 cells' invasion, gelatinase production and cell adhesive abilities. Western blot assay was utilized to detect the effects of si-CD147 on focal adhesion kinase (FAK), vinculiln and mitogen-activated protein kinase (MAPK) expression in SMMC-7721 cells.</p> <p>Results</p> <p>Downregulation of CD147 gene induced the alteration of SMMC-7721 cell cytoskeleton including actin, microtubule and vimentin filaments, and inhibited gelatinase production and expression, cells invasion, FAK and vinculin expression. si-CD147 also blocked SMMC-7721 cells adhesion to collagen IV and phosphorylation level of SAPK/JNKs. SAPK/JNKs inhibitor SP600125 inhibited gelatinase production and expression.</p> <p>Conclusion</p> <p>CD147 is required for normal tumor cell architecture and cell invasion. Downregulation of CD147 affects HCC cell structure and function. Moreover, the alteration of cell behavior may be related to SAPK/JNK Pathway. siRNA against CD147 may be a possible new approach for HCC gene therapy.</p