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provides coniferyl ferulate(CAS#:245724-07-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
A crucial aim upon the completion of the human genome is the verification and functional annotation of all predicted genes and their protein products. Here we describe the mapping of peptides derived from accurate interpretations of protein tandem mass spectrometry (MS) data to eukaryotic genomes and the generation of an expandable resource for integration of data from many diverse proteomics experiments. Furthermore, we demonstrate that peptide identifications obtained from high-throughput proteomics can be integrated on a large scale with the human genome. This resource could serve as an expandable repository for MS-derived proteome information.
Integration with the human genome of peptide sequences obtained by high-throughput mass spectrometry
Frank Desiere, Eric W Deutsch, Alexey I Nesvizhskii, Parag Mallick, Nichole L King, Jimmy K Eng, Alan Aderem, Rose Boyle, Erich Brunner, Samuel Donohoe, Nelson Fausto, Ernst Hafen, Lee Hood, Michael G Katze, Kathleen A Kennedy, Floyd Kregenow, Hookeun Lee, Biaoyang Lin, Dan Martin, Jeffrey A Ranish, David J Rawlings, Lawrence E Samelson, Yuzuru Shiio, Julian D Watts, Bernd Wollscheid, Michael E Wright, Wei Yan, Lihong Yang, Eugene C Yi, Hui Zhang, Ruedi Aebersold
This retrospective cohort study evaluated the risk of prostate cancer associated with sitagliptin use in Taiwanese male patients with type 2 diabetes mellitus by using the reimbursement databases of the National Health Insurance. Male patients with newly diagnosed type 2 diabetes mellitus at an age ≥25 years between 1999 and 2010 were recruited. A total of 37,924 ever users of sitagliptin and 426,276 never users were followed until December 31, 2011. The treatment effect of sitagliptin (for ever versus never users, and for tertiles of cumulative duration of therapy) was estimated by Cox regression incorporated with the inverse probability of treatment weighting using propensity score. Analyses were also conducted in a 1:1 matched pair cohort based on 8 digits of propensity score. Results showed that during follow-up, 84 ever users and 2,549 never users were diagnosed of prostate cancer, representing an incidence of 140.74 and 240.17 per 100,000 person-years, respectively. The hazard ratio (95% confidence intervals) for ever users versus never users was 0.613 (0.493-0.763). The respective hazard ratio for the first, second, and third tertile of cumulative duration of sitagliptin use <5.9, 5.9-12.7 and >12.7 months was 0.853 (0.601-1.210), 0.840 (0.598-1.179) and 0.304 (0.191-0.483), respectively; and was 0.856 (0.603-1.214), 0.695 (0.475-1.016) and 0.410 (0.277-0.608) for cumulative dose <15,000, 15,000-33,600 and >33,600 mg, respectively. Findings were supported by analyses in the matched cohort. In conclusion, sitagliptin significantly reduces the risk of prostate cancer, especially when the cumulative duration is >12.7 months or the cumulative dose >33,600 mg.
incretin, National Health Insurance, prostate cancer, sitagliptin, Taiwan
Sitagliptin may reduce prostate cancer risk in male patients with type 2 diabetes
2017 Mar 21
Fibroblast growth factor‐2 (FGF2) is a potent angiogenic growth factor. Here, gene expression profiling of FGF2‐stimulated microvascular endothelial cells revealed, together with a prominent pro‐angiogenic profile, a pro‐inflammatory signature characterized by the up‐regulation of pro‐inflammatory cytokine/chemokines and their receptors, endothelial cell adhesion molecules and members of the eicosanoid pathway. Real‐time quantitative PCR demonstrated early induction of most of the FGF2‐induced, inflammation‐related genes. Accordingly, chick embryo chorioallantoic membrane (CAM) and murine Matrigel plug angiogenesis assays demonstrated a significant monocyte/macrophage infiltrate in the areas of FGF2‐driven neovascularization. Similar results were obtained when the conditioned medium (CM) of FGF2‐stimulated endothelial cells was delivered onto the CAM, suggesting that FGF2‐upregulated chemoattractants mediate the inflammatory response. Importantly, FGF2‐triggered new blood vessel formation was significantly reduced in phosphatidylinositol 3‐kinase‐γ null mice exhibiting defective leucocyte migration or in clodronate liposome‐treated, macrophage‐depleted mice. Furthermore, the viral pan‐chemokine antagonist M3 inhibited the angiogenic and inflammatory responses induced by the CM of FGF2‐stimulated endothelial cells and impaired FGF2‐driven neovascularization in the CAM assay. These findings point to inflammatory chemokines as early mediators of FGF2‐driven angiogenesis and indicate a non‐redundant role for inflammatory cells in the neovascularization process elicited by the growth factor.
angiogenesis, chemokines, FGF, inflammation, macrophages
A pro‐inflammatory signature mediates FGF2‐induced angiogenesis
German Andres, Daria Leali, Stefania Mitola, Daniela Coltrini, Maura Camozzi, Michela Corsini, Mirella Belleri, Emilio Hirsch, Reto A. Schwendener, Gerhard Christofori, Antonio Alcamì, Marco Presta