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5,7-Dihydroxy-3,4‘,8-trimethoxyflavone

$780

  • Brand : BIOFRON

  • Catalogue Number : AV-C10166

  • Specification : 98%

  • CAS number : 1570-09-8

  • Formula : C18H16O7

  • Molecular Weight : 344.3

  • PUBCHEM ID : 13916278

  • Volume : 5mg

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Catalogue Number

AV-C10166

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

344.3

Appearance

Yellow powder

Botanical Source

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=CC=C(C=C1)C2=C(C(=O)C3=C(O2)C(=C(C=C3O)O)OC)OC

Synonyms

5,7-Dihydroxy-3,4',8-trimethoxyflavone/5,7-Dihydroxy-3,8,4'-trimethoxyflavone/4H-1-Benzopyran-4-one, 5,7-dihydroxy-3,8-dimethoxy-2-(4-methoxyphenyl)-/W1654/3,8,4'-Trimethylherbacetin/5,7-Dihydroxy-3,8-dimethoxy-2-(4-methoxyphenyl)-4H-chromen-4-one/Herbacetin 3,8,4'-trimethyl ether

IUPAC Name

5,7-dihydroxy-3,8-dimethoxy-2-(4-methoxyphenyl)chromen-4-one

Density

1.5±0.1 g/cm3

Solubility

mild hypothermia, mathematical modeling, CHO cells, N?linked glycosylation, galactosylation, flux balance analysis, monoclonal antibody

Flash Point

212.2±23.6 °C

Boiling Point

577.3±50.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

RXQVMRRNRHSOTC-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:1570-09-8) 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

27869292

Abstract

Despite the positive effects of mild hypothermic conditions on monoclonal antibody (mAb) productivity (q mAb) during mammalian cell culture, the impact of reduced culture temperature on mAb Fc?glycosylation and the mechanism behind changes in the glycan composition are not fully established. The lack of knowledge about the regulation of dynamic intracellular processes under mild hypothermia restricts bioprocess optimization. To address this issue, a mathematical model that quantitatively describes Chinese hamster ovary (CHO) cell behavior and metabolism, mAb synthesis and mAb N?linked glycosylation profile before and after the induction of mild hypothermia is constructed. Results from this study show that the model is capable of representing experimental results well in all of the aspects mentioned above, including the N?linked glycosylation profile of mAb produced under mild hypothermia. Most importantly, comparison between model simulation results for different culture temperatures suggests the reduced rates of nucleotide sugar donor production and galactosyltransferase (GalT) expression to be critical contributing factors that determine the variation in Fc?glycan profiles between physiological and mild hypothermic conditions in stable CHO transfectants. This is then confirmed using experimental measurements of GalT expression levels, thereby closing the loop between the experimental and the computational system. The identification of bottlenecks within CHO cell metabolism under mild hypothermic conditions will aid bioprocess optimization, for example, by tailoring feeding strategies to improve NSD production, or manipulating the expression of specific glycosyltransferases through cell line engineering. Biotechnol. Bioeng. 2017;114: 1570-1582. ? 2016 The Authors. Biotechnology and Bioengineering Published by Wiley Periodicals Inc.

KEYWORDS

mild hypothermia, mathematical modeling, CHO cells, N?linked glycosylation, galactosylation, flux balance analysis, monoclonal antibody

Title

Model?based investigation of intracellular processes determining antibody Fc?glycosylation under mild hypothermia

Author

Si Nga Sou, 1 , 2 , 3 Philip M. Jedrzejewski, 3 Ken Lee, 4 Christopher Sellick, 4 Karen M. Polizzi, 1 , 2 and Cleo Kontoravdicorresponding author 3

Publish date

2017 Jul;

PMID

7929833

Abstract

Insulin-mediated vasodilation has been proposed as a determinant of in vivo insulin sensitivity. We tested whether sustained vasodilation with adenosine could overcome the muscle insulin resistance present in mildly overweight patients with essential hypertension. Using the forearm technique, we measured the response to a 40-min local intraarterial infusion of adenosine given under fasting conditions (n = 6) or superimposed on a euglycemic insulin clamp (n = 8). In the fasting state, adenosine-induced vasodilation (forearm blood flow from 2.6 +/- 0.6 to 6.0 +/- 1.2 ml min-1dl-1, P < 0.001) was associated with a 45% rise in muscle oxygen consumption (5.9 +/- 1.0 vs 8.6 +/- 1.7 mumol min-1dl-1, P < 0.05), and a doubling of forearm glucose uptake (0.47 +/- 0.15 to 1.01 +/- 0.28 mumol min-1dl-1, P < 0.05). The latter effect remained significant also when expressed as a ratio to concomitant oxygen balance (0.08 +/- 0.03 vs 0.13 +/- 0.04 mumol mumol-1, P < 0.05), whereas for all other metabolites (lactate, pyruvate, FFA, glycerol, citrate, and beta-hydroxybutyrate) this ratio remained unchanged. During euglycemic hyperinsulinemia, whole-body glucose disposal was stimulated (to 19 +/- 3 mumol min-1kg-1), but forearm blood flow did not increase significantly above baseline (2.9 +/- 0.2 vs 3.1 +/- 0.2 ml min-1dl-1, P = NS). Forearm oxygen balance increased (by 30%, P < 0.05) and forearm glucose uptake rose fourfold (from 0.5 to 2.3 mumol min-1dl-1, P < 0.05). Superimposing an adenosine infusion into one forearm resulted in a 100% increase in blood flow (from 2.9 +/- 0.2 to 6.1 +/- 0.9 ml min-1dl-1, P < 0.001); there was, however, no further stimulation of oxygen or glucose uptake compared with the control forearm. During the clamp, the ratio of glucose to oxygen uptake was similar in the control and in the infused forearms (0.27 +/- 0.11 and 0.23 +/- 0.09, respectively), and was not altered by adenosine (0.31 +/- 0.9 and 0.29 +/- 0.10). We conclude that in insulin-re15-76sistant patients with hypertension, adenosine-induced vasodilation recruits oxidative muscle tissues and exerts a modest, direct metabolic effect to promote muscle glucose uptake in the fasting state. Despite these effects, however, adenosine does not overcome muscle insulin resistance.

Title

Insulin resistance and vasodilation in essential hypertension. Studies with adenosine.

Author

A Natali, R Bonadonna, D Santoro, A Q Galvan, S Baldi, S Frascerra, C Palombo, S Ghione, and E Ferrannini

Publish date

1994 Oct;

PMID

23463013

Abstract

Phantom pain after arm amputation is widely believed to arise from maladaptive cortical reorganization, triggered by loss of sensory input. We instead propose that chronic phantom pain experience drives plasticity by maintaining local cortical representations and disrupting inter-regional connectivity. Here we show that, while loss of sensory input is generally characterized by structural and functional degeneration in the deprived sensorimotor cortex, the experience of persistent pain is associated with preserved structure and functional organization in the former hand area. Furthermore, consistent with the isolated nature of phantom experience, phantom pain is associated with reduced inter-regional functional connectivity in the primary sensorimotor cortex. We therefore propose that contrary to the maladaptive model, cortical plasticity associated with phantom pain is driven by powerful and long-lasting subjective sensory experience, such as triggered by nociceptive or top-down inputs. Our results prompt a revisiting of the link between phantom pain and brain organization.

Title

Phantom pain is associated with preserved structure and function in the former hand area

Author

Tamar R. Makin,a,1 Jan Scholz,1,2 Nicola Filippini,1,3 David Henderson Slater,4 Irene Tracey,1,5 and Heidi Johansen-Berg1

Publish date

2013 Mar 5;


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