Red crystalline powder/Yellow powder
Psoralea corylifolia Linn.
batracyclin/4,2'-dihydroxy-4'-methoxy-5'-prenylchalcone/2-Propen-1-one, 1-[2-hydroxy-4-methoxy-5-(3-methyl-2-buten-1-yl)phenyl]-3-(4-hydroxyphenyl)-, (2E)-/(2E)-1-[2-Hydroxy-4-methoxy-5-(3-methyl-2-buten-1-yl)phenyl]-3-(4-hydroxyphenyl)-2-propen-1-one/bavachalcone/Batracylin/4'-O-Methyl-bavachalcon/Daniquidone/(2E)-1-[2-Hydroxy-4-methoxy-5-(3-methylbut-2-en-1-yl)phenyl]-3-(4-hydroxyphenyl)prop-2-en-1-one/4'-O-Methylbroussochalcone B
Methanol; Ethyl Acetate
552.1±50.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:20784-60-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Graft contracture is a common problem associated with the regeneration processes of tissue-engineered bladders. Currently, most strategies used for incorporating bioactive molecules into biomaterial designs do not work during all phases of tissue regeneration. In this study, we used a growth factor-PLGA nanoparticle thermo-sensitive gel system (i.e., BAM with incorporated VEGF and bFGF-loaded PLGA nanoparticles and mixed with a hydrophilic gel) to promote bladder tissue regeneration in a rabbit model. At 4 and 12 weeks after surgery, contracture rate assessment and histological examination were conducted to evaluate bladder tissue regeneration. The results indicated that the functional composite scaffold continuously and effectively released VEGF and bFGF and promoted bladder reconstruction with a significant decrease in graft contracture. In addition, the number and arrangement of regenerated urothelial cells and smooth muscle cells as well as microvascular density and maturity were improved in the VEGF/bFGF nanoparticle group compared with the single factor VEGF or bFGF nanoparticle group and BAM alone. The nanoparticle thermo-sensitive gel system, which exhibited favourable performance, may effectively inhibit graft contracture and promote bladder tissue regeneration in rabbits.
Varieties of congenital and acquired bladder anomalies and diseases, such as neurogenic bladder, bladder exstrophy, or posterior urethral valves, may require augmentation cystoplasty1. The current primary standard of surgical treatment is bladder replacement or augmentation with gastrointestinal segments. However, the substitution of intestinal tissue within the urinary tract is fraught with many potential complications, such as urolithiasis, infection, metabolic abnormalities and even malignancy2,3. Therefore, urologists have long sought an ideal and optimal substitute to serve as a platform for reliable, complete and functional bladder tissue regeneration.
Bladder acellular matrix (BAM) is an extensively studied scaffold that has been utilized to support bladder augmentation in various animal models and several clinical trials4,5. Naturally derived BAM retains a porous three-dimensional structure, as well as collagen, elastin, fibronectin and growth factors, which are important for orchestrating the adherence, proliferation, migration and differentiation of multi-layered urothelial cells (UCs), smooth muscle cells (SMCs), endothelial cells and others6,7. However, the pure degradable scaffold alone does not provide a satisfactory result because it can elicit various negative effects, such as fibroblast depiction, collagen deposition, scar formation, and grafting contracture, over time8,9,10,11. Tissues thicker than 0.8 mm or with an area greater than 3 mm2 require vascularization to provide cells with adequate nutrients and oxygen and to remove waste and damaged products12,13. The early and rapid building of a mature vascular network is critical to facilitate grafting of organoids and to support long-term tissue survival14. Growth factors are considered to be crucial regulatory molecules throughout the course of tissue regeneration. One strategy to improve the outcome of bladder tissue regeneration is to incorporate a BAM with biologically active growth factors15. Many incorporation methods, such as injection, rehydration, and incubation, have been demonstrated to enhance the ability of the BAM to mediate bladder tissue regeneration in the short term (2 or 3 weeks)16,17,18,19,20,21,22. However, the introduced growth factors may not have a noticeable effect for a long time. The release pattern of growth factors must correlate with all phases of bladder tissue regeneration.
In our previous study, we have designed a thermal-responsive BAM system containing hydrogel-entrapped protein nanoparticles to promote angiogenesis of the BAM23. Instead of directly embedding these bioactive molecules into the BAM, our in vitro and in vivo studies have demonstrated that this novel system provided a histocompatible environment and acted as an effective drug carrier, exhibiting sustained delivery without an acute inflammatory reaction or toxic manifestation. Furthermore, numerous studies have demonstrated that vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) may enhance angiogenesis and smooth muscle regeneration in bladder replacement models18,24,25. In the present study, we used a poly(lactic-co-glycolic acid) (PLGA) nanoparticle (NP)-modified BAM to co-deliver VEGF and bFGF in an effort to rapidly restore vascular networks and to effectively inhibit contracture in augmented bladders. The scaffolds were analysed in vitro for protein release. Additionally, the modified scaffolds were implanted in the bladders of rabbits for up to 12 weeks. The implanted scaffolds were analysed for graft contracture, host cell infiltration, vascularization, collagen degradation and deposition, and regenerated smooth muscle strip contractility.
Co-delivery of VEGF and bFGF via a PLGA nanoparticle-modified BAM for effective contracture inhibition of regenerated bladder tissue in rabbits
Xincheng Jiang,1,* Houwei Lin,1,* Dapeng Jiang,1 Guofeng Xu,1 Xiaoliang Fang,1 Lei He,1 Maosheng Xu,1 Bingqiang Tang,1 Zhiyong Wang,2 Daxiang Cui,3 Fang Chen,4 and Hongquan Genga,1
2016 Feb 8
Ribose-1,5-bisphosphate isomerase (R15Pi) is a novel enzyme recently identified as a member of an AMP metabolic pathway in archaea. The enzyme converts d-ribose 1,5-bisphosphate into ribulose 1,5-bisphosphate, providing the substrate for archaeal ribulose-1,5-bisphosphate carboxylase/oxygenases. We here report the crystal structures of R15Pi from Thermococcus kodakarensis KOD1 (Tk-R15Pi) with and without its substrate or product. Tk-R15Pi is a hexameric enzyme formed by the trimerization of dimer units. Biochemical analyses show that Tk-R15Pi only accepts the α-anomer of d-ribose 1,5-bisphosphate and that Cys133 and Asp202 residues are essential for ribulose 1,5-bisphosphate production. Comparison of the determined structures reveals that the unliganded and product-binding structures are in an open form, whereas the substrate-binding structure adopts a closed form, indicating domain movement upon substrate binding. The conformational change to the closed form optimizes active site configuration and also isolates the active site from the solvent, which may allow deprotonation of Cys133 and protonation of Asp202 to occur. The structural features of the substrate-binding form and biochemical evidence lead us to propose that the isomerase reaction proceeds via a cis-phosphoenolate intermediate.
Archaea, Crystal Structure, Enzyme Mechanisms, Protein Conformation, Rubisco, AMP Metabolism, Carbon Fixation, cis-Phosphoenolate Intermediate, Ribose-1,5-bisphosphate Isomerase
Dynamic, Ligand-dependent Conformational Change Triggers Reaction of Ribose-1,5-bisphosphate Isomerase from Thermococcus kodakarensis KOD1*
Akira Nakamura,‡ Masahiro Fujihashi,‡ Riku Aono,§ Takaaki Sato,§ Yosuke Nishiba,‡ Shosuke Yoshida,§ Ayumu Yano,§ Haruyuki Atomi,§ Tadayuki Imanaka,¶ and Kunio Miki‡,1
2012 Apr 17.
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic destructive inflammation in synovial joints. To date, many studies explored the associations between tumor necrosis factor alpha inducible protein 3 (TNFAIP3) gene rs6920220, rs2230926, and rs5029937 polymorphisms and the risk of rheumatoid arthritis (RA), but with contradictory results. We therefore conducted a comprehensive meta-analysis to address the associations. We searched in the databases of PubMed and Embase. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by the Stata 11.0 software. A total of 21 case-control studies for these three single nucleotide polymorphisms (SNPs) were included in this meta-analysis. Meta-analysis indicated that TNFAIP3 gene rs6920220, rs2230926, and rs5029937 polymorphisms were associated with the increased risk of RA. Stratification analysis of ethnicity found that rs6920220 and rs5029937 polymorphisms increased the risk of RA among Caucasians, while rs2230926 polymorphism increased the risk of RA among Asians. In summary, this meta-analysis confirms that TNFAIP3 gene polymorphisms may play important roles in the pathogenesis of RA.
TNFAIP3, single nucleotide polymorphism, rheumatoid arthritis, meta-analysis
Three single nucleotide polymorphisms of TNFAIP3 gene increase the risk of rheumatoid arthritis
Nan Shen,#1 Yuan Ruan,#2,# Yajun Lu,3 Xuefeng Jiang,4 Huiqing Sun,4 Gongming Gao,5 Luming Nong,5 and Kewei Ren4
2017 Mar 28