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8-epidiosbulbin E acetate

$600

  • Brand : BIOFRON

  • Catalogue Number : BD-P0270

  • Specification : 98.0%(HPLC)

  • CAS number : 91095-48-6

  • Formula : C21H24O7

  • Molecular Weight : 388.416

  • PUBCHEM ID : 134715250

  • Volume : 25mg

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Catalogue Number

BD-P0270

Analysis Method

HPLC,NMR,MS

Specification

98.0%(HPLC)

Storage

2-8°C

Molecular Weight

388.416

Appearance

Powder

Botanical Source

Structure Type

Diterpenoids

Category

SMILES

CC(=O)OC1CC2C(=O)OC(CC2(C3C1C4CC(C3)OC4=O)C)C5=COC=C5

Synonyms

[(1R,2S,3S,5S,8S,10S,11R,13R)-8-(furan-3-yl)-10-methyl-6,15-dioxo-7,14-dioxatetracyclo[11.2.1.02,11.05,10]hexadecan-3-yl] acetate

IUPAC Name

[(1R,2S,3S,5S,8S,10S,11R,13R)-8-(furan-3-yl)-10-methyl-6,15-dioxo-7,14-dioxatetracyclo[11.2.1.02,11.05,10]hexadecan-3-yl] acetate

Applications

Density

Solubility

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

Flash Point

Boiling Point

Melting Point

InChl

InChI=1S/C21H24O7/c1-10(22)26-16-7-15-20(24)28-17(11-3-4-25-9-11)8-21(15,2)14-6-12-5-13(18(14)16)19(23)27-12/h3-4,9,12-18H,5-8H2,1-2H3/t12-,13+,14+,15+,16-,17-,18+,21-/m0/s1

InChl Key

DYSOIAQEKRDXRB-GFTCARDDSA-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#:91095-48-6) 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

26227554

Abstract

Objective
To test for gender-differences in the relation between mothers’ antenatal anxiety and infants’ body weight during gestation, at birth, and at 1-month of age.

Methods
Two hundred and twelve randomly-recruited women were divided into two groups: Controls (n = 105) and Anxious Group (n = 107) based on a standard cut-off of the Beck Anxiety Inventory. Outcome measures were Fetal Weight derived from biometrics obtained from an ultrasound scan in the 3rd trimester and infants’ weight at birth and at 1-month of age, both obtained from medical records.

Results
Multivariate analyses showed main effects of Gender on infants’ birth weight (P = .001) and on infants’ weight at 1-month of age (P = .004), but no main effects of Anxiety Group at any time-point. Gender x Anxiety Group interactions at all three time points (Fetal weight: P = .05; Birth weight: P = .03; 1-month of age: P = .10) reflected gender differences (males > females) among infants in the anxious group, but not among controls. Distinct trends regarding same sex comparisons across groups (Control vs. Anxiety) were in line with predictions (male controls < male anxious; female controls > females anxious). Controlling for Postpartum Anxiety and Antenatal and Postpartum Depression in the models did not affect primary results.

Conclusion
Gender differences in fetal and birth weight were more substantial among infants of anxious mothers than among controls due to the seemingly accelerated growth of “anxious” males and the diminution of weight among “anxious” females.

KEYWORDS

Antenatal Anxiety, Gender, Fetal programming, Fetal Weight, Sexual Dimorphism

Title

Relation between maternal antenatal anxiety and infants’ weight depends on infants’ sex: A longitudinal study from late gestation to 1-month post birth

Author

Marsha Kaitz, PhD,corresponding authorb David Mankuta, MD,c Ann Marie Rokem, MA,d and Stephen V. Faraone, PhDe

Publish date

2016 Dec 1.

PMID

24221408

Abstract

Purpose
This study examined the likelihood of giving birth to a daughter as a function of women’s exposure to four categories of stressors: Childhood Trauma, Adult Trauma, Chronic Stressors, and Recent (adverse) Life Events. Hypothesis 1 stated that that exposure to Recent Life Events (near conception) and to childhood traumas would increase women’s chances of having a girl baby. Hypothesis 2 stated that the relation between stress and gender outcome is mediated by persistent PTSD symptoms.

Method
The final sample was comprised of 225 women. The design was Prospective Observational. At first contact, women were retained if they were < 27 weeks pregnant and met initial inclusion criteria. In interview 2, at 27-30 weeks, women were excluded for positive diagnoses of anxiety disorders besides PTSD with or without depression (Structured Clinical Interview for DSM disorders). In interview 3 (30-34 weeks), reports on stress categories (Social Stress Indicator Questionnaire, SSI) and PTSD symptoms (Post Traumatic Checklist) were obtained. Infant Gender was obtained from medical records. The relation between stress categories and the distribution of girl/boy infants was examined with Chi Squares and Logistic Regression analyses. Mediation was tested with the macro PROCESS (Hayes 2012). Results Childhood Trauma was the only stress category that increased the odds of having a girl; with an odds ratio of > 3.0 for women who had been exposed to more than two such events. PTSD symptoms (partially) mediated the relation between Childhood Trauma and infant gender.

Conclusions
Findings suggest that women’s exposure to childhood trauma contributes to the determination of the sex ratio at birth and that PTSD symptoms are part of the cause.

KEYWORDS

Sex ratio, Prenatal stress, Childhood trauma, PTSD, Pregnancy, Gender

Title

Exposure to Childhood Traumas Ups the Odds of Giving Birth to Daughters

Author

Marsha Kaitz, PhD, Ann Marie Rokem, MA, David Mankuta, MD, Maayan Davidov, PhD, and Stephen V. Faraone, PhD

Publish date

2015 Apr 1.

PMID

22031191

Abstract

Precis: Many genes are differentially expressed in normal compared to anencephalic human fetal adrenals (HFAs), especially the Fras-1-related extracellular matrix protein (FREM2) gene. FREM2 expression appears to be regulated by adrenocorticotrophic hormone (ACTH). Context: The expression profiles of genes responsible for cortical growth and zonation in the HFA gland are poorly characterized. The neural tube disorder anencephaly is associated with fetal adrenal hypoplasia with a large size reduction of the fetal zone of the HFA. Objective: To determine gene expression profile differences in the adrenals of anencephalic compared to normal HFAs to identify genes that may play important roles in adrenal development. Design and Methods: Fresh tissues were obtained at the time of autopsy from normal and anencephalic human fetuses delivered at mid-gestation. The following techniques were used: cell culture, messenger RNA (mRNA) extraction, microarray analysis, complementary DNA (cDNA) synthesis, quantitative real-time reverse transcriptase polymerase chain reaction (QT-PCR). Results: We identified over 40 genes expressed at levels 4-fold or greater in the normal versus anencephalic HFAs and that 28 genes were expressed at increased levels in the anencephalic HFA. The expression of FREM2 at approximately 40-fold greater levels in the normal HFA compared to the HFA of anencephalic fetuses was confirmed by QT-PCR. Expression of FREM2 in the kidney was not significantly different between normal and anencephalic fetuses. In cultured HFA cells, ACTH treatment for 48 hours increased the expression of FREM2 and a gene responsive to ACTH, CYP17, but not tyrosine hydroxylase. Conclusions: Abnormal expression of many genes may be involved in the adrenal hypoplasia seen in anencephaly. FREM2 appears to be regulated by ACTH and is the most differentially expressed gene, which may be important in the development and function of the HFA, particularly the fetal zone of the HFA.

KEYWORDS

fetal adrenal gland, anencephaly, FREM2, Fras-1-related extracellular matrix protein, ACTH

Title

Differential Gene Expression in the Adrenals of Normal and Anencephalic Fetuses and Studies Focused on the Fras-1-Related Extracellular Matrix Protein (FREM2) Gene

Author

Christine W. Mansfield, MD,1 Bruce R. Carr, MD,1 Ona M. Faye-Petersen, MD,2 Dongquan Chen, PhD, MSHI,3 Yewei Xing, PhD,4 William E. Rainey, PhD,4 and C. Richard Parker, Jr, PhD5

Publish date

2011 Nov;