Catalogue Number
BD-P0771
Analysis Method
HPLC,NMR,MS
Specification
98.0%(HPLC)
Storage
2-8°C
Molecular Weight
Appearance
Powder
Botanical Source
Structure Type
Phenols
Category
SMILES
CC1=CC(=O)C2=C(C3=C(C=C(C=C3C=C2O1)OC)OC4C(C(C(C(O4)COC5C(C(C(C(O5)CO)O)OC6C(C(C(C(O6)COC7C(C(C(C(O7)CO)O)O)O)O)O)O)O)O)O)O)O
Synonyms
6-[(2S,3R,4S,5S,6R)-6-[[(2R,3R,4S,5R,6R)-3,5-dihydroxy-6-(hydroxymethyl)-4-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxymethyl]oxan-2-yl]oxyoxan-2-yl]oxymethyl]-3,4,5-trihydroxyoxan-2-yl]oxy-5-hydroxy-8-methoxy-2-methylbenzo[g]chromen-4-one
IUPAC Name
Density
1.468g/cm3
Solubility
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Flash Point
Boiling Point
Melting Point
InChl
InChI=1S/C39H52O25/c1-11-3-14(42)22-15(58-11)5-12-4-13(55-2)6-16(21(12)27(22)47)59-38-32(52)29(49)24(44)19(62-38)10-57-37-34(54)35(26(46)18(8-41)61-37)64-39-33(53)30(50)25(45)20(63-39)9-56-36-31(51)28(48)23(43)17(7-40)60-36/h3-6,17-20,23-26,28-41,43-54H,7-10H2,1-2H3/t17-,18-,19-,20-,23-,24-,25-,26-,28+,29+,30+,31-,32-,33-,34-,35+,36-,37-,38-,39+/m1/s1
InChl Key
HFJDWELARBQGBQ-PFLZFKCOSA-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#:218155-40-9) 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.
31660890
Background
We examined 15 years of key performance indicators (KPIs) of the population-based mammography screening programme (PMSP) in Flanders, Belgium.
Methods
Individual screening data were linked to the national cancer registry to obtain oncological follow-up. We benchmarked crude KPI results against KPI-targets set by the European guidelines and KPI results of other national screening programmes. Temporal trends were examined by plotting age-standardised KPIs against the year of screening and estimating the Average Annual Percentage Change (AAPC).
Results
PMSP coverage increased significantly over the period of 15 years (+ 7.5% AAPC), but the increase fell to + 1.6% after invitation coverage was maximised. In 2016, PMSP coverage was at 50.0% and opportunistic coverage was at 14.1%, resulting in a total coverage by screening of 64.2%. The response to the invitations was 49.8% in 2016, without a trend. Recall rate decreased significantly (AAPC -1.5% & -5.0% in initial and subsequent regular screenings respectively) while cancer detection remained stable (AAPC 0.0%). The result was an increased positive predictive value (AAPC + 3.8%). Overall programme sensitivity was stable and was at 65.1% in 2014.
In initial screens of 2015, the proportion of DCIS, tumours stage II+, and node negative invasive cancers was 18.2, 31.2, and 61.6% respectively. In subsequent regular screens of 2015, those proportions were 14.0, 24.8, and 65.4% respectively. Trends were not significant.
Conclusion
Besides a suboptimal attendance rate, most KPIs in the Flemish PMSP meet EU benchmark targets. Nonetheless, there are several priorities for further investigation such as a critical evaluation of strategies to increase screening participation, organising a biennial radiological review of interval cancers, analysing the effect that preceding opportunistic screening has on the KPI for initial screenings, and efforts to estimate the impact on breast cancer mortality.
Flemish breast cancer screening programme: 15 years of key performance indicators (2002-2016)
M. Goossens,corresponding author1,2 I. De Brabander,3 J. De Greve,1 C. Van Ongeval,4 P. Martens,2 E. Van Limbergen,4,2 and E. Kellen4,2
2019;
30984317
Stroke is one of the most devastating pathologies of the early twenty-first century demonstrating 1-month case-fatality rates ranging from 13 to 35% worldwide. Though the majority of cases do occur in individuals at an advanced age, a persistently increasing portion of the patient cohorts is affected early in life. Current studies provide alarming statistics for the incidence of “young” strokes including adolescents. Young stroke is a multifactorial disease involving genetic predisposition but also a number of modifiable factors, the synergic combination of which potentiates the risks. The article analyzes the prevalence and impacts of “traditional” risk factors such as sedentary lifestyle, smoking, abnormal alcohol consumption, drug abuse, overweight, hypertension, abnormal sleep patterns, and usage of hormonal contraceptives, among others. Further, less explored risks such as primary vascular dysregulation and associated symptoms characteristic for Flammer syndrome (FS) are considered, and the relevance of the FS phenotype for the stroke predisposition at young age is hypothesized. Considering the high prevalence of known genetic and modifiable risk factors in the overall predisposition to the young stroke, the risk mitigating measures are recommended including innovative screening programs by application of specialized questionnaires and biomarker panels as well as educational programs adapted to the target audiences such as children, adolescents, and young adults.
Young adults, Stroke, Risk factors, Individualized patient profile, Etiology, Vascular, Abnormal BMI, Blood flow, Microcirculation, Life style, Sleep patterns, Migraine, Hormonal regulation, Psychology, Stress, Screening program, Flammer syndrome, Phenotype, Questionnaire, Risk assessment, Baroreceptor sensitivity, Cardiac, Circadian rhythm, Tinnitus, Thermoregulation, Altered sensation, Body dehydration, Predictive preventive personalized medicine
Risks associated with the stroke predisposition at young age: facts and hypotheses in light of individualized predictive and preventive approach
Jiri Polivka, Jr,1,2,3 Jiri Polivka,3 Martin Pesta,2,4 Vladimir Rohan,3 Libuse Celedova,5 Smit Mahajani,6 Ondrej Topolcan,7 and Olga Golubnitschajacorresponding author8,9,10
2019 Mar;
16358416
Communication between the central nervous and the immune system occurs through chemical messengers secreted by nerve cells, endocrine organs, or immune cells. Psychological stressors can disrupt these networks. We have previously observed that disruption of the neuroendocrine immune system adversely influences a broad range of physiological processes including wound healing. Migration of neutrophils to the wound site is an early event that induces a transcriptional activation program, which regulates cellular fate and function, and promotes wound healing. In this study, we have sought to identify stress-sensitive transcripts in wound site neutrophils. A skin blister model was used to collect wound fluid and wound site neutrophils from four young men, experiencing or not examination stress. Self-reported stress was recorded using the Beck Depression Inventory. Stress decreased growth hormone levels at the wound site and was related to impaired wound healing in all subjects. High density microarray analyses were performed using RNA from wound site neutrophils. Results show that psychological stress had an overall suppressive effect on the neutrophil transcriptome. Of the 22,283 transcripts screened, 0.5% were downregulated whereas only under 0.3% were induced by stress in all four out of four subjects. Functionally, stress tilted the genomic balance towards genes encoding proteins responsible for cell cycle arrest, death, and inflammation. Further effort to gain a more comprehensive understanding of the functional significance of such behavior-genome interaction is warranted.
Wound healing, Skin, Microarray, Clinical, Gene
Wound Site Neutrophil Transcriptome in Response to Psychological Stress in Young Men
Sashwati Roy,* Savita Khanna,* Pier-En Yeh,† Cameron Rink,* William B. Malarkey,†‡§¶# Janice Kiecolt-Glaser,§ Bryon Laskowski,† Ronald Glaser,†¶# and Chandan K. Sen*
2005