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Magnolignan A

$730

  • Brand : BIOFRON

  • Catalogue Number : AV-B02996

  • Specification : 95%

  • CAS number : 93673-81-5

  • Formula : C18H20O4

  • Molecular Weight : 300.35

  • PUBCHEM ID : 5319201

  • Volume : 5mg

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Catalogue Number

AV-B02996

Analysis Method

HPLC,NMR,MS

Specification

95%

Storage

2-8°C

Molecular Weight

300.35

Appearance

Oil

Botanical Source

Structure Type

Lignans

Category

Standards;Natural Pytochemical;API

SMILES

C=CCC1=CC(=C(C=C1)O)C2=C(C=CC(=C2)CC(CO)O)O

Synonyms

[1,1'-Biphenyl]-2,2'-diol, 5-(2,3-dihydroxypropyl)-5'-(2-propen-1-yl)-/5-Allyl-5'-(2,3-dihydroxypropyl)-2,2'-biphenyldiol

IUPAC Name

3-[4-hydroxy-3-(2-hydroxy-5-prop-2-enylphenyl)phenyl]propane-1,2-diol

Applications

Density

1.2±0.1 g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

244.5±23.3 °C

Boiling Point

518.2±45.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C18H20O4/c1-2-3-12-4-6-17(21)15(9-12)16-10-13(5-7-18(16)22)8-14(20)11-19/h2,4-7,9-10,14,19-22H,1,3,8,11H2/t14-/m1/s1

InChl Key

ORPULAPYNPMMAQ-CQSZACIVSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:93673-81-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

28870089

Abstract

Mitogen-activated protein kinase (MAPK) signaling has been implicated in a wide range of neuronal processes, including development, plasticity, and viability. One of the principal downstream targets of both the extracellular signal-regulated kinase/MAPK pathway and the p38 MAPK pathway is Mitogen- and Stress-activated protein Kinase 1 (MSK1). Here, we sought to understand the role that MSK1 plays in neuroprotection against excitotoxic stimulation in the hippocampus. To this end, we utilized immunohistochemical labeling, a MSK1 null mouse line, cell viability assays, and array-based profiling approaches. Initially, we show that MSK1 is broadly expressed within the major neuronal cell layers of the hippocampus and that status epilepticus drives acute induction of MSK1 activation. In response to the status epilepticus paradigm, MSK1 KO mice exhibited a striking increase in vulnerability to pilocarpine-evoked cell death within the CA1 and CA3 cell layers. Further, cultured MSK1 null neurons exhibited a heighted level of N-methyl-D-aspartate-evoked excitotoxicity relative to wild-type neurons, as assessed using the lactate dehydrogenase assay. Given these findings, we examined the hippocampal transcriptional profile of MSK1 null mice. Affymetrix array profiling revealed that MSK1 deletion led to the significant (>1.25-fold) downregulation of 130 genes and an upregulation of 145 genes. Notably, functional analysis indicated that a subset of these genes contribute to neuroprotective signaling networks. Together, these data provide important new insights into the mechanism by which the MAPK/MSK1 signaling cassette confers neuroprotection against excitotoxic insults. Approaches designed to upregulate or mimic the functional effects of MSK1 may prove beneficial against an array of degenerative processes resulting from excitotoxic insults.

KEYWORDS

cell death, excitotoxicity, hippocampus, MAPK, MSK1, neuroprotection

Title

Mitogen- and Stress-Activated Protein Kinase 1 Regulates Status Epilepticus-Evoked Cell Death in the Hippocampus

Author

Yun-Sik Choi,1 Paul Horning,2 Sydney Aten,2 Kate Karelina,2 Diego Alzate-Correa,3 J. Simon C. Arthur,4 Kari R. Hoyt,3 and Karl Obrietan2

Publish date

2017 Sep-Oct

PMID

25559822

Abstract

Background: This is the 31st Annual Report of the American Association of Poison Control Centers’ (AAPCC) National Poison Data System (NPDS). As of January 1, 2013, 57 of the nation’s poison centers (PCs) uploaded case data automatically to NPDS. The upload interval was 8.08 [7.10, 11.63] (median [25%, 75%]) minutes, creating a near real-time national exposure and information database and surveillance system.

Methodology: We analyzed the case data tabulating specific indices from NPDS. The methodology was similar to that of previous years. Where changes were introduced, the differences are identified. Poison center (PC) cases with medical outcomes of death were evaluated by a team of 38 medical and clinical toxicologist reviewers using an ordinal scale of 1-6 to assess the Relative Contribution to Fatality (RCF) of the exposure to the death.

Results: In 2013, 3,060,122 closed encounters were logged by NPDS: 2,188,013 human exposures, 59,496 animal exposures, 806,347 information calls, 6,116 human-confirmed nonexposures, and 150 animal-confirmed nonexposures. Total encounters showed a 9.3% decline from 2012, while health care facility human exposure calls were essentially flat, decreasing by 0.1%.All information calls decreased 21.4% and health care facility (HCF) information calls decreased 8.5%, medication identification requests (drug ID) decreased 26.8%, and human exposures reported to US PCs decreased 3.8%. Human exposures with less serious outcomes have decreased 3.7% per year since 2008 while those with more serious outcomes (moderate, major or death) have increased by 4.7% per year since 2000.

The top five substance classes most frequently involved in all human exposures were analgesics (11.5%), cosmetics/personal care products (7.7%), household cleaning substances (7.6%), sedatives/hypnotics/antipsychotics (5.9%), and antidepressants (4.2%). Sedative/hypnotics/antipsychotics exposures as a class increased most rapidly (2,559 calls/year) over the last 13 years for cases showing more serious outcomes. The top five most common exposures in children of 5 years or less were cosmetics/personal care products (13.8%), household cleaning substances (10.4%), analgesics (9.8%), foreign bodies/toys/miscellaneous (6.9%), and topical preparations (6.1%). Drug identification requests comprised 50.7% of all information calls. NPDS documented 2,477 human exposures resulting in death with 2,113 human fatalities judged related (RCF of 1, undoubtedly responsible; 2, probably responsible; or 3, contributory).

Conclusions: These data support the continued value of PC expertise and need for specialized medical toxicology information to manage the more severe exposures, despite a decrease in calls involving less severe exposures. Unintentional and intentional exposures continue to be a significant cause of morbidity and mortality in the United States. The near real-time, always current status of NPDS represents a national public health resource to collect and monitor US exposure cases and information calls. The continuing mission of NPDS is to provide a nationwide infrastructure for public health surveillance for all types of exposures, public health event identification, resilience response and situational awareness tracking. NPDS is a model system for the nation and global public health.

Title

2013 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st Annual Report

Author

James B. Mowry, * Daniel A. Spyker, Louis R. Cantilena, Jr, Naya McMillan, and Marsha Ford

Publish date

2014 Dec 1;

PMID

28316832

Abstract

In the title mononuclear complex, [Ru(C14H20O2)2(C10H8N2)], the RuII ion has a distorted octa­hedral coordination environment defined by two N atoms of the chelating 2,2′-bi­pyridine ligand and four O atoms from two 3,5-di-tert-butyl-o-benzo­quinone ligands. In the crystal, the complex mol­ecules are linked by inter­molecular C?H?O hydrogen bonds and π-π stacking inter­actions between the 2,2′-bi­pyridine ligands [centroid-centroid distance = 3.538?(3)?a], resulting in a layer structure extending parallel to the ab plane

KEYWORDS

crystal structure, Ru(II) complex, π-π stacking, 3,5-di-tert-butyl-o-benzo­quinone, 2,2′-bi­pyridine

Title

Crystal structure of (2,2′-bi­pyridine-κ2 N,N′)bis­(3,5-di-tert-butyl-o-benzo­quinonato-κ2 O,O′)ruthenium(II)

Author

Md. Serajul Haque Faizi,a Akram Ali,b and Vadim A. Potaskalovc,*

Publish date

2017 Mar 1;