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Aloeresin D

$672

  • Brand : BIOFRON

  • Catalogue Number : BD-P0065

  • Specification : 98.5%(HPLC)

  • CAS number : 105317-67-7

  • PUBCHEM ID : 14211225

  • Volume : 25mg

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Catalogue Number

BD-P0065

Analysis Method

HPLC,NMR,MS

Specification

98.5%(HPLC)

Storage

2-8°C

Molecular Weight

Appearance

Powder

Botanical Source

Structure Type

Chromones

Category

Standards;Natural Pytochemical;API

SMILES

CC1=CC(=C(C2=C1C(=O)C=C(O2)CC(C)O)C3C(C(C(C(O3)CO)O)O)OC(=O)C=CC4=CC=C(C=C4)O)OC

Synonyms

(1S)-1,5-Anhydro-2-O-[(2E)-3-(4-hydroxyphenyl)-2-propenoyl]-1-{2-[(2R)-2-hydroxypropyl]-7-methoxy-5-methyl-4-oxo-4H-chromen-8-yl}-D-glucitol/D-Glucitol, 1,5-anhydro-2-O-[(2E)-3-(4-hydroxyphenyl)-1-oxo-2-propen-1-yl]-1-C-[2-[(2R)-2-hydroxypropyl]-7-methoxy-5-methyl-4-oxo-4H-1-benzopyran-8-yl]-, (1S)-

IUPAC Name

[(2S,3R,4S,5S,6R)-4,5-dihydroxy-6-(hydroxymethyl)-2-[2-[(2R)-2-hydroxypropyl]-7-methoxy-5-methyl-4-oxochromen-8-yl]oxan-3-yl] (E)-3-(4-hydroxyphenyl)prop-2-enoate

Applications

Aloeresin D is a chromone glycoside isolated from Aloe vera, inhibits β-Secretase (BACE1) activity, with an IC50 of 39 μM[1].

Density

1.5±0.1 g/cm3

Solubility

Methanol

Flash Point

261.7±26.4 °C

Boiling Point

796.8±60.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C29H32O11/c1-14-10-20(37-3)24(27-23(14)19(33)12-18(38-27)11-15(2)31)28-29(26(36)25(35)21(13-30)39-28)40-22(34)9-6-16-4-7-17(32)8-5-16/h4-10,12,15,21,25-26,28-32,35-36H,11,13H2,1-3H3/b9-6+/t15-,21-,25-,26+,28+,29-/m1/s1

InChl Key

OUGNWRCWQLUXHX-ACWXGELRSA-N

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:105317-67-7) 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

29477216

Abstract

Aims
Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice. Patients presenting with AF are often admitted to hospital for rhythm or rate control, symptom management, and/or anticoagulation. We investigated temporal trends in AF hospitalizations in United States from 1996 to 2010.

Methods
Data were obtained from the National Hospital Discharge Survey (NHDS), a national probability sample survey of discharges conducted annually by National Center for Health Statistics. Because of the survey design, sampling weights were applied to the raw NHDS data to produce national estimates. Hospitalizations with a primary diagnosis of AF were identified using International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) code of 427.31. Weighted least squares regression was used to test for linear trends in the number of AF admissions, length of stay, and inpatient mortality. We further stratified AF admissions based on patients’ age, gender, and race.

Results
Admissions for a primary diagnosis of AF increased from approximately 286,000 in 1996 to about 410,000 in 2010 with a significant linear trend (β = 9470 additional admissions per year, p < 0.001). The trend of increased AF admissions was uniform across patient sub-groups. Overall, mean length of stay for AF admissions was 3.75 days, and this remained relatively stable over time (β = 0.002 days, p = 0.884). Inpatient mortality was 0.96% and also remained stable over time (β = 0.031%, p = 0.181). Conclusion Our data demonstrate an increase in the number of AF admissions but constant length of stay and mortality over time.

KEYWORDS

Atrial fibrillation, Hospitalization, Length of stay, Mortality

Title

Trends in atrial fibrillation hospitalizations in the United States: A report using data from the National Hospital Discharge Survey

Author

Muhammad Umer Nisar,a Muhammad Bilal Munir,b,∗ Michael S. Sharbaugh,a Floyd W. Thoma,a Andrew D. Althouse,a and Samir Sabaa

Publish date

2018 Jan-Feb

PMID

29343433

Abstract

Group 3 innate lymphoid cells (ILC3s) sense environmental signals and are critical for tissue integrity in the intestine. Yet, which signals are sensed and what receptors control ILC3 function remain poorly understood. Here, we show that ILC3s with a lymphoid-tissue-inducer (LTi) phenotype expressed G-protein-coupled receptor 183 (GPR183) and migrated to its oxysterol ligand 7α,25-hydroxycholesterol (7α,25-OHC). In mice lacking Gpr183 or 7α,25-OHC, ILC3s failed to localize to cryptopatches (CPs) and isolated lymphoid follicles (ILFs). Gpr183 deficiency in ILC3s caused a defect in CP and ILF formation in the colon, but not in the small intestine. Localized oxysterol production by fibroblastic stromal cells provided an essential signal for colonic lymphoid tissue development, and inflammation-induced increased oxysterol production caused colitis through GPR183-mediated cell recruitment. Our findings show that GPR183 promotes lymphoid organ development and indicate that oxysterol-GPR183-dependent positioning within tissues controls ILC3 activity and intestinal homeostasis.

KEYWORDS

innate lymphoid cells, oxysterols, GPR183, EBI2, cell migration, colon, lymphoid tissue, inflammation

Title

Oxysterol Sensing through the Receptor GPR183 Promotes the Lymphoid-Tissue-Inducing Function of Innate Lymphoid Cells and Colonic Inflammation

Author

Johanna Emgard,1,11 Hana Kammoun,1,11 Bethania Garcia-Cassani,2 Julie Chesne,2 Sara M. Parigi,3 Jean-Marie Jacob,4,5 Hung-Wei Cheng,6 Elza Evren,1 Srustidhar Das,3 Paulo Czarnewski,3 Natalie Sleiers,1 Felipe Melo-Gonzalez,7 Egle Kvedaraite,1 Mattias Svensson,1 Elke Scandella,6 Matthew R. Hepworth,7 Samuel Huber,8 Burkhard Ludewig,6 Lucie Peduto,4,5 Eduardo J. Villablanca,3 Henrique Veiga-Fernandes,2 João P. Pereira,9 Richard A. Flavell,9,10,∗ and Tim Willinger1,9,12,13,∗∗

Publish date

2018 Jan 16

PMID

23986601

Abstract

Myxomatosis is a rapidly lethal disease of European rabbits that is caused by myxoma virus (MYXV). The introduction of a South American strain of MYXV into the European rabbit population of Australia is the classic case of host-pathogen coevolution following cross-species transmission. The most virulent strains of MYXV for European rabbits are the Californian viruses, found in the Pacific states of the United States and the Baja Peninsula, Mexico. The natural host of Californian MYXV is the brush rabbit, Sylvilagus bachmani. We determined the complete sequence of the MSW strain of Californian MYXV and performed a comparative analysis with other MYXV genomes. The MSW genome is larger than that of the South American Lausanne (type) strain of MYXV due to an expansion of the terminal inverted repeats (TIRs) of the genome, with duplication of the M156R, M154L, M153R, M152R, and M151R genes and part of the M150R gene from the right-hand (RH) end of the genome at the left-hand (LH) TIR. Despite the extreme virulence of MSW, no novel genes were identified; five genes were disrupted by multiple indels or mutations to the ATG start codon, including two genes, M008.1L/R and M152R, with major virulence functions in European rabbits, and a sixth gene, M000.5L/R, was absent. The loss of these gene functions suggests that S. bachmani is a relatively recent host for MYXV and that duplication of virulence genes in the TIRs, gene loss, or sequence variation in other genes can compensate for the loss of M008.1L/R and M152R in infections of European rabbits.

Title

Comparative Analysis of the Complete Genome Sequence of the California MSW Strain of Myxoma Virus Reveals Potential Host Adaptations

Author

Peter J. Kerr,a Matthew B. Rogers,b,c Adam Fitch,c Jay V. DePasse,c Isabella M. Cattadori,d Peter J. Hudson,d David C. Tscharke,e Edward C. Holmes,f,g and Elodie Ghedincorresponding authorb,c

Publish date

2013 Nov