Acanthoppanax gracilistylus W. W. Smith.
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
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provides coniferyl ferulate(CAS#:19889-23-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Genetic research of elite athletic performance has been hindered by the complex phenotype and the relatively small effect size of the identified genetic variants. The aims of this study were to identify genetic predisposition to elite athletic performance by investigating genetically-influenced metabolites that discriminate elite athletes from non-elite athletes and to identify those associated with endurance sports. By conducting a genome wide association study with high-resolution metabolomics profiling in 490 elite athletes, common variant metabolic quantitative trait loci (mQTLs) were identified and compared with previously identified mQTLs in non-elite athletes. Among the identified mQTLs, those associated with endurance metabolites were determined. Two novel genetic loci in FOLH1 and VNN1 are reported in association with N-acetyl-aspartyl-glutamate and Linoleoyl ethanolamide, respectively. When focusing on endurance metabolites, one novel mQTL linking androstenediol (3alpha, 17alpha) monosulfate and SULT2A1 was identified. Potential interactions between the novel identified mQTLs and exercise are highlighted. This is the first report of common variant mQTLs linked to elite athletic performance and endurance sports with potential applications in biomarker discovery in elite athletic candidates, non-conventional anti-doping analytical approaches and therapeutic strategies.
Subject terms: Genome-wide association studies, Predictive marker
Metabolic GWAS of elite athletes reveals novel genetically-influenced metabolites associated with athletic performance
Fatima Al-Khelaifi,1,2 Ilhame Diboun,3 Francesco Donati,4 Francesco Botre,4 David Abraham,2 Aroon Hingorani,5 Omar Albagha,3,6 Costas Georgakopoulos,1 Karsten Suhre,7 Noha A. Yousri,#8,9 and Mohamed A. Elrayesscorresponding author#10
To assess if commercially sponsored trials are associated with higher success rates than publicly-sponsored trials.
Study Design and Settings
We undertook a systematic review of all consecutive, published and unpublished phase III cancer randomized controlled trials (RCTs) conducted by GlaxoSmithKline (GSK) and the NCIC Clinical Trials Group (CTG). We included all phase III cancer RCTs assessing treatment superiority from 1980 to 2010. Three metrics were assessed to determine treatment successes: (1) the proportion of statistically significant trials favouring the experimental treatment, (2) the proportion of the trials in which new treatments were considered superior according to the investigators, and (3) quantitative synthesis of data for primary outcomes as defined in each trial.
GSK conducted 40 cancer RCTs accruing 19,889 patients and CTG conducted 77 trials enrolling 33,260 patients. 42% (99%CI 24 to 60) of the results were statistically significant favouring experimental treatments in GSK compared to 25% (99%CI 13 to 37) in the CTG cohort (RR = 1.68; p = 0.04). Investigators concluded that new treatments were superior to standard treatments in 80% of GSK compared to 44% of CTG trials (RR = 1.81; p<0.001). Meta-analysis of the primary outcome indicated larger effects in GSK trials (odds ratio = 0.61 [99%CI 0.47-0.78] compared to 0.86 [0.74-1.00]; p = 0.003). However, testing for the effect of treatment over time indicated that treatment success has become comparable in the last decade. Conclusions While overall industry sponsorship is associated with higher success rates than publicly-sponsored trials, the difference seems to have disappeared over time.
Treatment Success in Cancer: Industry Compared to Publicly Sponsored Randomized Controlled Trials
Benjamin Djulbegovic, 1 , 2 , 3 , * Ambuj Kumar, 1 , 2 , 3 Branko Miladinovic, 1 , 2 Tea Reljic, 1 , 2 Sanja Galeb, 3 Asmita Mhaskar, 1 , 2 Rahul Mhaskar, 1 , 2 Iztok Hozo, 4 Dongsheng Tu, 5 , 6 Heather A. Stanton, 5 Christopher M. Booth, 5 , 6 , 7 and Ralph M. Meyer 5 , 6 , 7
Photosensitizing fluorescent proteins, which generate reactive oxygen species (ROS) upon light irradiation, are useful for spatiotemporal protein inactivation and cell ablation. They give us clues about protein function, intracellular signaling pathways and intercellular interactions. Since ROS generation of a photosensitizer is specifically controlled by certain excitation wavelengths, utilizing colour variants of photosensitizing protein would allow multi-spatiotemporal control of inactivation. To expand the colour palette of photosensitizing protein, here we developed SuperNova Green from its red predecessor, SuperNova.
SuperNova Green is able to produce ROS spatiotemporally upon blue light irradiation. Based on protein characterization, SuperNova Green produces insignificant amounts of singlet oxygen and predominantly produces superoxide and its derivatives. We utilized SuperNova Green to specifically inactivate the pleckstrin homology domain of phospholipase C-δ1 and to ablate cancer cells in vitro. As a proof of concept for multi-spatiotemporal control of inactivation, we demonstrate that SuperNova Green can be used with its red variant, SuperNova, to perform independent protein inactivation or cell ablation studies in a spatiotemporal manner by selective light irradiation.
Development of SuperNova Green has expanded the photosensitizing protein toolbox to optogenetically control protein inactivation and cell ablation.
Electronic supplementary material
The online version of this article (10.1186/s12915-018-0514-7) contains supplementary material, which is available to authorized users.
Photosensitizer, Superoxide, CALI, ROS, Cell ablation, Protein inactivation, Green fluorescent protein, Pleckstrin homology domain
Green monomeric photosensitizing fluorescent protein for photo-inducible protein inactivation and cell ablation
Yemima Dani Riani,1 Tomoki Matsuda,1,2 Kiwamu Takemoto,3 and Takeharu Nagaicorresponding author1,2