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Phellodendrine chloride

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-P2008

  • Specification : 98%

  • CAS number : 104112-82-5

  • Formula : C20H24NO4.Cl

  • Molecular Weight : 377.87

  • PUBCHEM ID : 59818

  • Volume : 20mg

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Catalogue Number

BF-P2008

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

377.87

Appearance

White cryst.

Botanical Source

Phellodendron chinense,Phellodendron amurense

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

C[N+]12CCC3=CC(=C(C=C3C1CC4=CC(=C(C=C4C2)OC)O)O)OC.[Cl-]

Synonyms

6H-Dibenzo[a,g]quinolizinium, 5,8,13,13a-tetrahydro-2,11-dihydroxy-3,10-dimethoxy-7-methyl-, chloride, (13aS)- (1:1)/(13aS)-2,11-Dihydroxy-3,10-dimethoxy-7-methyl-5,8,13,13a-tetrahydro-6H-isoquinolino[3,2-a]isoquinolinium chloride

IUPAC Name

(13aS)-3,10-dimethoxy-7-methyl-6,8,13,13a-tetrahydro-5H-isoquinolino[2,1-b]isoquinolin-7-ium-2,11-diol;chloride

Density

Solubility

Methanol; Ethanol; Water

Flash Point

Boiling Point

Melting Point

249-251℃ (methanol )

InChl

InChI=1S/C20H23NO4.ClH/c1-21-5-4-12-8-19(24-2)18(23)10-15(12)16(21)6-13-7-17(22)20(25-3)9-14(13)11-21;/h7-10,16H,4-6,11H2,1-3H3,(H-,22,23);1H/t16-,21?;/m0./s1

InChl Key

DGLDSNPMIYUWGN-OOJQBDKLSA-N

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:104112-82-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

23514470

Abstract

We investigate the reversible diffusion-influenced reaction of an isolated pair in the presence of a non-Markovian generalization of the backreaction boundary condition in two space dimensions. Following earlier work by Agmon and Weiss, we consider residence time probability densities that decay slower than an exponential and that are characterized by a single parameter 0 < σ ⩽ 1. We calculate an exact expression for a Green’s function of the two-dimensional diffusion equation subject to a non-Markovian backreaction boundary condition that is valid for arbitrary σ and for all times. We use the obtained expression to derive the survival probability for the initially unbound pair and we calculate an exact expression for the probability S(t|*) that the initially bound particle is unbound. Finally, we obtain an approximate solution for long times. In particular, we show that the ultimate fate of the bound state is complete dissociation, as in the Markovian case. However, the limiting value is approached quite differently: Instead of a ∼t−1 decay, we obtain 1 − S(t|*) ∼ t−σln t. The derived expressions should be relevant for a better understanding of reversible membrane-bound reactions in cell biology.

Title

Theory of reversible diffusion-influenced reactions with non-Markovian dissociation in two space dimensions

Author

Thorsten Prustela) and Martin Meier-Schellersheimb)

Publish date

2013 Mar 13.

PMID

29654185

Title

Redefinition and Unification of the SXT/R391 Family of Integrative and Conjugative Elements

Author

Audrey Bioteau,a Romain Durand,a and Vincent Burruscorresponding authora

Publish date

2018 Jun 18

PMID

29654185

Abstract

Integrative and conjugative elements (ICEs) of the SXT/R391 family are key drivers of the spread of antibiotic resistance in Vibrio cholerae, the infectious agent of cholera, and other pathogenic bacteria. The SXT/R391 family of ICEs was defined based on the conservation of a core set of 52 genes and site-specific integration into the 5′ end of the chromosomal gene prfC. Hence, the integrase gene int has been intensively used as a marker to detect SXT/R391 ICEs in clinical isolates. ICEs sharing most core genes but differing by their integration site and integrase gene have been recently reported and excluded from the SXT/R391 family. Here we explored the prevalence and diversity of atypical ICEs in GenBank databases and their relationship with typical SXT/R391 ICEs. We found atypical ICEs in V. cholerae isolates that predate the emergence and expansion of typical SXT/R391 ICEs in the mid-1980s in seventh-pandemic toxigenic V. cholerae strains O1 and O139. Our analyses revealed that while atypical ICEs are not associated with antibiotic resistance genes, they often carry cation efflux pumps, suggesting heavy metal resistance. Atypical ICEs constitute a polyphyletic group likely because of occasional recombination events with typical ICEs. Furthermore, we show that the alternative integration and excision genes of atypical ICEs remain under the control of SetCD, the main activator of the conjugative functions of SXT/R391 ICEs. Together, these observations indicate that substitution of the integration/excision module and change of specificity of integration do not preclude atypical ICEs from inclusion into the SXT/R391 family.

IMPORTANCE Vibrio cholerae is the causative agent of cholera, an acute intestinal infection that remains to this day a world public health threat. Integrative and conjugative elements (ICEs) of the SXT/R391 family have played a major role in spreading antimicrobial resistance in seventh-pandemic V. cholerae but also in several species of Enterobacteriaceae. Most epidemiological surveys use the integrase gene as a marker to screen for SXT/R391 ICEs in clinical or environmental strains. With the recent reports of closely related elements that carry an alternative integrase gene, it became urgent to investigate whether ICEs that have been left out of the family are a liability for the accuracy of such screenings. In this study, based on comparative genomics, we broaden the SXT/R391 family of ICEs to include atypical ICEs that are often associated with heavy metal resistance.

KEYWORDS

antibiotic resistance, conjugation, entry exclusion, integrative and conjugative element, Vibrio cholerae, genetic recombination, site-specific recombination

Title

Redefinition and Unification of the SXT/R391 Family of Integrative and Conjugative Elements

Author

Audrey Bioteau,a Romain Durand,a and Vincent Burruscorresponding authora

Publish date

2018 Apr 13.


Description :

The defensive effect of phellodendrine against AAPH-induced oxidative stress through regulating the AKT/NF-κB pathway in zebrafish embryos. PUMID/DOI:27234894 Life Sci.?2016 Jul 15;157:97-106.? AIMS:This study is to investigate the effect of phellodendrine (PHE) against AAPH-induced oxidative stress and find out the biological mechanism of PHE by using the zebrafish embryo model.MAIN METHODS:After treatments by AAPH or PHE, the mortality and heartbeat of zebrafish embryos were recorded and the production of reactive oxygen species (ROS), lipid-peroxidation and the rate of cell death were detected by fluorescence spectrophotometry respectively. Whereafter, the pathways of PHE against AAPH-induced oxidative stress were screened by inhibitors to explore its biological mechanism. The related genes and proteins expressions were analyzed by real-time quantitative reverse-transcription polymerase-chain-reaction (qRT-PCR) and western blotting.KEY FINDINGS:The PHE obviously improved the decreased survival rate and abnormally elevated heart-beating rate of zebrafish embryos caused by AAPH. Especially 200μg/mL of PHE make the survival rate increased to 90.26±1.40% at 72hfp and the heartbeat back to normal. Besides, AAPH caused a significant increase in the production of reactive oxygen species (ROS), lipid-peroxidation and cell death rate, all of which could be decreased after PHE treatment dose-dependently. And PHE exerted the protective activity against AAPH-induced oxidative stress through down-regulating AKT phosphorylation and NF-kB3 expression, which associate with modulation of IKK phosphorylation in zebrafish embryos.SIGNIFICANCE:The PHE showed a good antioxidant effect in vivo, and the mechanism has been stated that the PHE can down-regulating AKT, IKK, NF-kB phosphorylation and COX-2 expression induced by AAPH. Moreover, the PHE also ameliorated the ROS-mediated inflammatory response.