Light yellow powder
4',6'-dimethoxy-2',4-dihydroxychalcone/Flavokavain C/1-(2-hydroxy-4,6-dimethoxy)phenyl-3-(4-hydroxy)phenyl-2-propen-1-one/2',4-Dihydroxy-4',6'-dimethoxychalcone/2'-hydroxy-4,6'-dimethoxychalcone/2-Propen-1-one, 1-(2-hydroxy-4,6-dimethoxyphenyl)-3-(4-hydroxyphenyl)-, (2E)-/(E)-1-(2-Hydroxy-4,6-dimethoxyphenyl)-3-(4-hydroxyphenyl)prop-2-en-1-one/2299311/(2E)-1-(2-Hydroxy-4,6-dimethoxyphenyl)-3-(4-hydroxyphenyl)-2-propen-1-one/Flavokawain C/Flavokawin C/flavokawin/(2E)-1-(2-Hydroxy-4,6-dimethoxyphenyl)-3-(4-hydroxyphenyl)prop-2-en-1-one/QR D1U1VR BQ DO1 FO1 &&E Form/4',6'-di-O-methylchalconaringenin
Flavokawain C is a natural chalcone found in Kava root. Flavokawain C exerts cytotoxicity against human cancer cell lines, with an IC50 of 12.75 μM for HCT 116 cells.
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
556.0±50.0 °C at 760 mmHg
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For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:37308-75-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
The flagellum of parasitic trypanosomes is a multifunctional appendage essential for its viability and infectivity. However, the biological mechanisms that make the flagellum so dynamic remains unexplored. No method is available to access and induce axonemal motility at will to decipher motility regulation in trypanosomes. For the first time we report the development of a detergent-extracted/demembranated ATP-reactivated model for studying flagellar motility in Leishmania. Flagellar beat parameters of reactivated parasites were similar to live ones. Using this model we discovered that cAMP (both exogenous and endogenous) induced flagellar wave reversal to a ciliary waveform in reactivated parasites via cAMP-dependent protein kinase A. The effect was reversible and highly specific. Such an effect of cAMP on the flagellar waveform has never been observed before in any organism. Flagellar wave reversal allows parasites to change direction of swimming. Our findings suggest a possible cAMP-dependent mechanism by which Leishmania responds to its surrounding microenvironment, necessary for its survival. Our demembranated-reactivated model not only serves as an important tool for functional studies of flagellated eukaryotic parasites but has the potential to understand ciliary motility regulation with possible implication on human ciliopathies.
Leishmaniasis represents a group of geographically widespread diseases caused by different species of kinetoplastid parasites of genus Leishmania1. These parasites lead a digenetic life in two specific hosts, the sandfly, where they proliferate as motile, flagellated promastigotes and in mammals (including humans) where they invade utilizing their flagellum and then grow intracellularly2. The flagellum of trypanosomes like Leishmania is unusual in that it generates flagellar waves that propagate proximally from the tip (tip-to-base) that pulls the cell forward. These waves are interrupted by abrupt ‘cilia-like’ distally propagating waves (base-to-tip) enabling the cell to change direction in response to an obstacle3,4. The physics of parasite motility has received interdisciplinary focus due to its importance in host-parasite interactions5. However, till date flagellar motility and its regulation in Leishmania remains poorly understood despite the importance in its survival and infectivity.
In the sandfly host, the flagellum performs several attachment mechanisms that allow the passage of the promastigotes to anterior parts of the gut6,7. This ensures the proper positioning of the parasites to be transmitted by the insect’s bite and is possibly directed by chemotaxis8. Once the promastigotes are transferred to the mammalian host, the vigorous and unusual oscillations of flagellar tip invades the macrophages, reorienting the parasite and damaging the macrophage plasma membrane2. This uptake is highly reduced in immobile parasites2. The Leishmania flagellum thus, is a highly versatile organelle that exhibits intricate environment triggered responses far beyond simple fluid swimming behaviour5. Studies of the flagellar ultrastructure have been possible in the related trypanosome Trypanosoma brucei using RNAi techniques9 which is not possible in Leishmania spp3. except only in L. braziliensis10. In humans, defects in cilia cause a group of severe diseases called ciliopathies11. These defects constitute both structural defects as well as defects in the motility of the cilia. Eukaryotic parasites like trypanosomes have served as attractive models for the study of such genetic defects in humans with extensive research on structure and assembly of the cilia12. However, there is no suitable model till date for the study of the signalling and regulatory mechanisms of ciliary motility in ciliopathies.
Most of our current understanding of the regulatory mechanism controlling flagellar and ciliary beating come from detergent-extracted/demembranated, ATP reactivation studies in organisms like sperms of sea urchins, Ciona, dog, bull, flagella of Chlamydomonas and cilia of Paramecium13,14,15,16,17,18. In 1983, Alexander and Burns, reported their inability to reactivate demembranated Leishmania flagella4. Since then, no report on reactivation of Leishmania flagella has been published. The only trypanosome to receive attention using detergent-extracted models were the non-parasitic protozoa of genus Crithidia19,20. The fact that the flagellum is important for the viability and infectivity of pathogenic parasites like Leishmania, makes the information known on the non-parasitic species unsuitable to study its role in host-parasite relationships3. The absence of reports elucidating the control mechanism of flagellar motility in Leishmania led us to questions like: can the demembranated Leishmania flagella be reactivated? If so then would it be possible to tease out the regulatory mechanisms of flagellar motility? We presume that such a reactivated model will allow numerous studies in the future elucidating leishmanial flagellar motility and associated functionality for its survival and infection. Such a model would also have the potential to study the signalling pathways that possibly malfunction in ciliopathies.
Reactivation of flagellar motility in demembranated Leishmania reveals role of cAMP in flagellar wave reversal to ciliary waveform
Aakash Gautam Mukhopadhyay1 and Chinmoy Sankar Deya,1
2016 Nov 16
It has been reported that peroxisome proliferator-activated receptor gamma (PPARG) and peroxisome proliferator-activated receptor gamma co-activator 1 (PPARGC1) family (e.g. PPARGC1A and PPARGC1B) are key agents in the development and pathophysiology of type 2 diabetes mellitus (T2DM). In this study, we designed a case-control study and selected PPARG rs1801282 C>G, PPARG rs3856806 C>T, PPARGC1A rs8192678 C>T, PPARGC1A rs2970847 C>T, PPARGC1A rs3736265 G>A, PPARGC1B rs7732671 G>C and PPARGC1B rs17572019 G>A polymorphisms to assess the relationship between these polymorphisms and T2DM using the SNPscan method. A total of 502 T2DM patients and 784 non-diabetic controls were enrolled. We found that PPARGC1A rs3736265 G>A polymorphism was correlated with a borderline decreased susceptibility of T2DM. In a subgroup analysis by age, sex, alcohol use, smoking status and body mass index, a significantly decreased risk of T2DM in <65 years and female groups was found. Haplotype comparison analysis indicated that CTTCGGG and CTCTGGG haplotypes with the order of PPARG rs1801282 C>G, PPARG rs3856806 C>T, PPARGC1A rs8192678 C>T, PPARGC1A rs2970847 C>T, PPARGC1A rs3736265 G>A, PPARGC1B rs7732671 G>C and PPARGC1B rs17572019 G>A polymorphisms in gene position significantly increased the risk of T2DM. However, CCCCACA haplotype conferred a decreased risk to T2DM. We also found that PPARGC1A rs3736265 A allele decreased the level of fasting plasma glucose (FPG), while increased the level of Triglyceride. In conclusion, Our findings suggest that variants of PPARGC1A rs3736265 G>A polymorphism decrease the level of FPG, improving the expectation of study in individual’s prevention strategies to T2DM.
PPARG, PPARGC1A, PPARGC1B, polymorphism, type 2 diabetes mellitus
PPARGC1A rs3736265 G>A polymorphism is associated with decreased risk of type 2 diabetes mellitus and fasting plasma glucose level
Li Zhu,#1 Qiuyu Huang,#2 Zhiqiang Xie,#3 Mingqiang Kang,4 Hao Ding,5 Boyang Chen,4 Yu Chen,6 Chao Liu,7 Yafeng Wang,8 and Weifeng Tang4
2017 Mar 17.
Implantation is a frequent procedure in orthopedic surgery, particularly in the aging population. However, it possesses the risk of infection and biofilm formation at the surgical site. This can cause unnecessary suffering to patients and burden on the healthcare system. Pure Mg, as a promising metal for biodegradable orthopedic implants, exhibits some antibacterial effects due to the alkaline pH produced during degradation. However, this antibacterial effect may not be sufficient in a dynamic environment, for example, the human body. The aim of this study was to increase the antibacterial properties under harsh and dynamic conditions by alloying silver metal with pure Mg as much as possible. Meanwhile, the Mg-Ag alloys should not show obvious cytotoxicity to human primary osteoblasts. Therefore, we studied the influence of the microstructure and the silver content on the degradation behavior, cytocompatibility, and antibacterial properties of Mg-Ag alloys in vitro. The results indicated that a higher silver content can increase the degradation rate of Mg-Ag alloys. However, the degradation rate could be reduced by eliminating the precipitates in the Mg-Ag alloys via T4 treatment. By controlling the microstructure and increasing the silver content, Mg-Ag alloys obtained good antibacterial properties in harsh and dynamic conditions but had almost equivalent cytocompatibility to human primary osteoblasts as pure Mg.
Influence of the Microstructure and Silver Content on Degradation, Cytocompatibility, and Antibacterial Properties of Magnesium-Silver Alloys In Vitro
Zhidan Liu, 1 Ronald Schade, 2 Berengere Luthringer, 1 Norbert Hort, 1 Holger Rothe, 2 Soren Muller, 3 Klaus Liefeith, 2 Regine Willumeit-Romer, 1 and Frank Feyerabend 1 , *
2017 Jun 22.