(E)-3-Hydroxy-5-methoxystilbene,(E)-3-Methoxy-5-(2-phenylethenyl)phenol,5-Methoxy-3-stilbenol/3-Methoxy-5-[(E)-2-phenylvinyl]phenol/3-Stilbenol, 5-methoxy-/Phenol, 3-methoxy-5- (2-phenylethenyl)-/O-Methyl-pinosylvin/pinosylvin monomethyl ether/3-methoxy-5-[(E)-2-phenylethenyl]phenol/pinosylvin-O-methyl ether/5-Hydroxy-3-methoxy-trans-stilben/5-Methoxy-3-stilbenol/Phenol, 3-methoxy-5-[(E)-2-phenylethenyl]-/3-hydroxy-5-methoxystilbene
405.8±24.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:35302-70-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Gallbladder cancer (GBC) is an aggressive malignancy. Although surgical resection may be curable, most patients are diagnosed at an advanced unresectable disease stage. Cholelithiasis is the major risk factor; however the pathogenesis of the disease, from gallstone cholecystitis to cancer, is still not understood. To understand the molecular genetic underpinnings of this cancer and explore novel therapeutic targets for GBC, we examined the key genes and pathways involved in GBC using RNA sequencing. We performed gene expression analysis of 32 cases of surgically-resected GBC along with normal gallbladder tissue controls. We observed that 519 genes were differentially expressed between GBC and normal GB mucosal controls. The liver X receptor (LXR)/retinoid X receptor (RXR) and farnesoid X receptor (FXR) /RXR pathways were the top canonical pathways involved in GBC. Key genes in these pathways, including SERPINB3 and KLK1, were overexpressed in GBC, especially in female GBC patients. Additionally, ApoA1 gene expression suppressed in GBC as compared with normal control tissues. LXR and FXR genes, known to be important in lipid metabolism also function as tumor suppressors and their down regulation appears to be critical for GBC pathogenesis. LXR agonists may have therapeutic value and as potential therapeutic targets.
RNA sequence, gallbladder cancer, liver X receptor, lipid metabolism pathways
RNA sequencing-based analysis of gallbladder cancer reveals the importance of the liver X receptor and lipid metabolism in gallbladder cancer
Mingxin Zuo,1 Asif Rashid,2 Ying Wang,3 Apurva Jain,1 Donghui Li,1 Anu Behari,4 Vinay Kumar Kapoor,4 Eugene J. Koay,5 Ping Chang,1 Jean Nicholas Vauthey,6 Yanan Li,1 Jaime A. Espinoza,7 Juan Carlos Roa,8 and Milind Javle1
2016 Jun 7
The ability of Mycoplasma hyopneumoniae to persist despite fluoroquinolone treatments was investigated with pigs. Groups of specific-pathogen-free pigs were experimentally infected with M. hyopneumoniae strain 116 and treated with marbofloxacin at the therapeutic dose (TD) or half of the therapeutic dose (TD/2) for 3 days. Results showed that, despite tissue penetration of marbofloxacin, particularly in the trachea and the tracheal secretions, the treatments did not have any influence on M. hyopneumoniae recovery from tracheal swabs. Mycoplasmas were also isolated from inner organs and tissues such as liver, spleen, kidneys, and bronchial lymph nodes. Recontamination of pigs via environment could not explain mycoplasma persistence after medication, as decontamination of pigs and allocation to a new disinfected environment did not have any significant effect on the phenomenon. A significant decrease in the susceptibility level to marbofloxacin of 12 mycoplasma clones reisolated after the treatments (TD/2 and TD) was observed. Two point mutations were found in the ParC quinolone resistance-determining region (QRDR) of DNA topoisomerase IV (Ser80→Phe and Asp84→Asn), and one point mutation was observed just behind the QRDR of ParC (Ala116→Glu). This is the first time that mutations in a gene coding for topoisomerase IV have been described for M. hyopneumoniae after in vivo marbofloxacin treatments in experimentally infected pigs. However, development of resistance is not sufficient to explain M. hyopneumoniae persistence in vivo since (i) marbofloxacin concentrations were above the marbofloxacin MIC of the wild-type strain and (ii) mycoplasmas reisolated after a single injection of marbofloxacin did not display an increased marbofloxacin MIC.
Persistence of Mycoplasma hyopneumoniae in Experimentally Infected Pigs after Marbofloxacin Treatment and Detection of Mutations in the parC Gene
J. Le Carrou,1 M. Laurentie,2 M. Kobisch,1 and A. V. Gautier-Bouchardon1,*
Pinnatoxin G (PnTX-G) is a marine toxin belonging to the class of cyclic imines and produced by the dinoflagellate Vulcanodinium rugosum. In spite of its strong toxicity to mice, leading to the classification of pinnatoxins into the class of “fast-acting toxins”, its hazard for human health has never been demonstrated. In this study, crude extracts of V. rugosum exhibited significant cytotoxicity against Neuro2A and KB cells. IC50 values of 0.38 µg mL−1 and 0.19 µg mL−1 were estimated on Neuro2A cells after only 24 h of incubation and on KB cells after 72 h of incubation, respectively. In the case of Caco-2 cells 48 h after exposure, the crude extract of V. rugosum induced cell cycle arrest accompanied by a dramatic increase in double strand DNA breaks, although only 40% cytotoxicity was observed at the highest concentration tested (5 µg mL−1). However, PnTX-G was not a potent cytotoxic compound as no reduction of the cell viability was observed on the different cell lines. Moreover, no effects on the cell cycle or DNA damage were observed following treatment of undifferentiated Caco-2 cells with PnTX-G. The crude extract of V. rugosum was thus partially purified using liquid-liquid partitioning and SPE clean-up. In vitro assays revealed strong activity of some fractions containing no PnTX-G. The crude extract and the most potent fraction were evaluated using full scan and tandem high resolution mass spectrometry. The dereplication revealed the presence of a major compound that could be putatively annotated as nakijiquinone A, N-carboxy-methyl-smenospongine or stachybotrin A, using the MarinLit™ database. Further investigations will be necessary to confirm the identity of the compounds responsible for the cytotoxicity and genotoxicity of the extracts of V. rugosum.
dereplication, cyclic imine, HRMS, bioactivity, pinnatoxins
Cytotoxicity, Fractionation and Dereplication of Extracts of the Dinoflagellate Vulcanodinium rugosum, a Producer of Pinnatoxin G
Marie Geiger,1,2,† Gwenaëlle Desanglois,3,† Kevin Hogeveen,3 Valerie Fessard,3 Thomas Leprêtre,1,2 Florence Mondeguer,1 Yann Guitton,1,2 Fabienne Herve,1 Veronique Sechet,1 Olivier Grovel,2 Yves-Francois Pouchus,2 and Philipp Hess1,*