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Noreugenin

$335

  • Brand : BIOFRON

  • Catalogue Number : BD-P0304

  • Specification : 98.0%(HPLC)

  • CAS number : 1013-69-0

  • Formula : C10H8O4

  • Molecular Weight : 192.2

  • Volume : 10mg

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Catalogue Number

BD-P0304

Analysis Method

HPLC,NMR,MS

Specification

98.0%(HPLC)

Storage

2-8°C

Molecular Weight

192.2

Appearance

Powder

Botanical Source

Structure Type

Flavonoids

Category

SMILES

CC1=CC(=O)C2=C(C=C(C=C2O1)O)O

Synonyms

5,7-dihydroxy-2-methylchromen-4-one

IUPAC Name

Applications

Density

1.5±0.1 g/cm3

Solubility

DMSO : 250 mg/mL (1300.93 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)

Flash Point

164.0±21.4 °C

Boiling Point

394.6±42.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C10H8O4/c1-5-2-7(12)10-8(13)3-6(11)4-9(10)14-5/h2-4,11,13H,1H3

InChl Key

NCUJRUDLFCGVOE-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

2914400000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:1013-69-0) 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

20815182

Abstract

Objective:
Establish the dose-response relationship between increasing sleep durations in a single night and recovery of neurobehavioral functions following chronic sleep restriction.

Design:
Intent-to-treat design in which subjects were randomized to 1 of 6 recovery sleep doses (0, 2, 4, 6, 8, or 10 h TIB) for 1 night following 5 nights of sleep restriction to 4 h TIB.

Setting:
Twelve consecutive days in a controlled laboratory environment.

Participants:
N = 159 healthy adults (aged 22-45 y), median = 29 y).

Interventions:
Following a week of home monitoring with actigraphy and 2 baseline nights of 10 h TIB, subjects were randomized to either sleep restriction to 4 h TIB per night for 5 nights followed by randomization to 1 of 6 nocturnal acute recovery sleep conditions (N = 142), or to a control condition involving 10 h TIB on all nights (N = 17).

Measurements and Results:
Primary neurobehavioral outcomes included lapses on the Psychomotor Vigilance Test (PVT), subjective sleepiness from the Karolinska Sleepiness Scale (KSS), and physiological sleepiness from a modified Maintenance of Wakefulness Test (MWT). Secondary outcomes included psychomotor and cognitive speed as measured by PVT fastest RTs and number correct on the Digit Symbol Substitution Task (DSST), respectively, and subjective fatigue from the Profile of Mood States (POMS). The dynamics of neurobehavioral outcomes following acute recovery sleep were statistically modeled across the 0 h-10 h recovery sleep doses. While TST, stage 2, REM sleep and NREM slow wave energy (SWE) increased linearly across recovery sleep doses, best-fitting neurobehavioral recovery functions were exponential across recovery sleep doses for PVT and KSS outcomes, and linear for the MWT. Analyses based on return to baseline and on estimated intersection with control condition means revealed recovery was incomplete at the 10 h TIB (8.96 h TST) for PVT performance, KSS sleepiness, and POMS fatigue. Both TST and SWE were elevated above baseline at the maximum recovery dose of 10 h TIB.

Conclusions:
Neurobehavioral deficits induced by 5 nights of sleep restricted to 4 h improved monotonically as acute recovery sleep dose increased, but some deficits remained after 10 h TIB for recovery. Complete recovery from such sleep restriction may require a longer sleep period during 1 night, and/or multiple nights of recovery sleep. It appears that acute recovery from chronic sleep restriction occurs as a result of elevated sleep pressure evident in both increased SWE and TST.

Citation:
Banks S; Van Dongen HPA; Maislin G; Dinges DF. Neurobehavioral dynamics following chronic sleep restriction: dose-response effects of one night for recovery. SLEEP 2010;33(8):1013-1026.

KEYWORDS

Recovery sleep, sleep dose response, chronic sleep restriction, neurobehavioral, homeostatic sleep drive, sleep duration, sleep deprivation, sleep loss, sleep need, PVT, KSS, MWT

Title

Neurobehavioral Dynamics Following Chronic Sleep Restriction: Dose-Response Effects of One Night for Recovery

Author

Siobhan Banks, PhD,1,2 Hans P. A. Van Dongen, PhD,3 Greg Maislin, MS, MA,4 and David F. Dinges, PhD1

Publish date

2010 Aug 1

PMID

31463572

Abstract

MSTO1 encodes a cytosolic mitochondrial fusion protein, misato homolog 1 or MSTO1. While the full genotype-phenotype spectrum remains to be explored, pathogenic variants in MSTO1 have recently been reported in a small number of patients presenting with a phenotype of cerebellar ataxia, congenital muscle involvement with histologic findings ranging from myopathic to dystrophic and pigmentary retinopathy. The proposed underlying pathogenic mechanism of MSTO1-related disease is suggestive of impaired mitochondrial fusion secondary to a loss of function of MSTO1. Disorders of mitochondrial fusion and fission have been shown to also lead to mitochondrial DNA (mtDNA) depletion, linking them to the mtDNA depletion syndromes, a clinically and genetically diverse class of mitochondrial diseases characterized by a reduction of cellular mtDNA content. However, the consequences of pathogenic variants in MSTO1 on mtDNA maintenance remain poorly understood. We present extensive phenotypic and genetic data from 12 independent families, including 15 new patients harbouring a broad array of bi-allelic MSTO1 pathogenic variants, and we provide functional characterization from seven MSTO1-related disease patient fibroblasts. Bi-allelic loss-of-function variants in MSTO1 manifest clinically with a remarkably consistent phenotype of childhood-onset muscular dystrophy, corticospinal tract dysfunction and early-onset non-progressive cerebellar atrophy. MSTO1 protein was not detectable in the cultured fibroblasts of all seven patients evaluated, suggesting that pathogenic variants result in a loss of protein expression and/or affect protein stability. Consistent with impaired mitochondrial fusion, mitochondrial networks in fibroblasts were found to be fragmented. Furthermore, all fibroblasts were found to have depletion of mtDNA ranging from 30 to 70% along with alterations to mtDNA nucleoids. Our data corroborate the role of MSTO1 as a mitochondrial fusion protein and highlight a previously unrecognized link to mtDNA regulation. As impaired mitochondrial fusion is a recognized cause of mtDNA depletion syndromes, this novel link to mtDNA depletion in patient fibroblasts suggests that MSTO1-deficiency should also be considered a mtDNA depletion syndrome. Thus, we provide mechanistic insight into the disease pathogenesis associated with MSTO1 mutations and further define the clinical spectrum and the natural history of MSTO1-related disease.

Electronic supplementary material
The online version of this article (10.1007/s00401-019-02059-z) contains supplementary material, which is available to authorized users.

KEYWORDS

MSTO1, Mitochondrial fusion, Cerebellar atrophy, Muscular dystrophy, MtDNA depletion

Title

MSTO1 mutations cause mtDNA depletion, manifesting as muscular dystrophy with cerebellar involvement

Author

S. Donkervoort,1 R. Sabouny,2 P. Yun,1 L. Gauquelin,3,4 K. R. Chao,5 Y. Hu,1 I. Al Khatib,2 A. Topf,6 P. Mohassel,1 B. B. Cummings,5 R. Kaur,1 D. Saade,1 S. A. Moore,7 L. B. Waddell,8,9 M. A. Farrar,10,11 J. K. Goodrich,5 P. Uapinyoying,1,33 S.H. S. Chan,12 A. Javed,13 M. E. Leach,1,14 P. Karachunski,15 J. Dalton,15 L. Medne,16 A. Harper,17 C. Thompson,18 I. Thiffault,19,20,21 S. Specht,6 R. E. Lamont,22 C. Saunders,19,20,21 H. Racher,22 F. P. Bernier,22 D. Mowat,11,23 N. Witting,24 J. Vissing,24 R. Hanson,21,25 K. A. Coffman,25,26 M. Hainlen,25,26 J. S. Parboosingh,22 A. Carnevale,3 G. Yoon,3,4 R. E. Schnur,27 Care4Rare Canada Consortium,29 K. M. Boycott,28,29 J. K. Mah,30 V. Straub,6,31 A. Reghan Foley,1 A. M. Innes,22 C. G. Bonnemann,corresponding author1 and T. E. Shuttcorresponding author2,32

Publish date

2019

PMID

23885028

Abstract

The suppressor of cytokine signaling 1 (SOCS1) has emerged as a critical inhibitory molecule for controlling the cytokine response and antigen presentation by dendritic cells (DCs), thereby regulating the magnitude of both innate and adaptive immunity. The aim of this study was to investigate whether the SOCS1 antagonist pJAK2(1001-1013) peptide can weaken or block the inhibition function of SOCS1 in DCs by evaluating the phenotype and cytokine production, antigen-presenting, and specific T-cell-activating capacities of DCs electroporated with human gastric cancer cell total RNA. Furthermore, STAT1 activation of the JAK/STAT signal pathway mediated by SOCS1 was analyzed by Western blotting. The results demonstrate that the SOCS1 antagonist pJAK2(1001-1013) peptide upregulated the expression of the maturation marker (CD83) and costimulatory molecule (CD86) of RNA-electroporated human monocyte-derived mature DCs (mDCs), potentiated the capacity of mDCs to induce T-cell proliferation, stimulated the secretion of proinflammatory cytokines, and enhanced the cytotoxicity of tumor cell antigen-specific CTLs activated by human gastric cancer cell total RNA-electroporated mDCs. Data from Western blot analysis indicate that STAT1 was further activated in pJAK2(1001-1013) peptide-loaded mDCs. These results imply that the SOCS1 antagonist pJAK2(1001-1013) peptide is an effective reagent for the enhancement of antigen-specific antitumor immunity by DCs.

Title

A Suppressor of Cytokine Signaling 1 Antagonist Enhances Antigen-Presenting Capacity and Tumor Cell Antigen-Specific Cytotoxic T Lymphocyte Responses by Human Monocyte-Derived Dendritic Cell

Author

Yongjun Wang,a Shengyu Wang,b Yuan Ding,a Yanhua Ye,a Yingyi Xu,a Huixiang He,a Qiaozhen Li,a Yanjun Mi,a Chunhua Guo,a Zhicai Lin,a Tao Liu,a Yaya Zhang,a Yuqiang Chen,corresponding authora and Jianghua Yancorresponding authorb

Publish date

2013 Sep;