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3篇 您的检索式:作者名="M.Milan"
    题名 作者 年代 出处 被引量
1Surface functionalization of acrylic based photocrosslinkable resin for 3D printing applications显示文摘The limited number of resins,available for stereolithography applications,is one of the key drivers in research applied to rapid prototyping.In this work an acrylic photocrosslinkable resin based on methyl methacrylate(MMA),butyl methacrylate(BMA)and poly(ethylene glycol)dimethacrylate(PEGDA)was developed with different composition and characterized in terms of mechanical,thermal and biological behaviour.Two different systems have been developed using different amount of reagent.The influence of every components have been evaluated on the final characteristic of the resin in order to optimize the final composition for applications in bone tissue engineering.The crosslinked materials showed good mechanical properties and thermal stabilities and moreover cytotoxicity test confirms good biocompatibility with no cytotoxic effect on cells metabolism.Moreover two different treatments have been proposed,using fetal bovine serum(FBS)and methanol(MeOH),in order to improve cell recognition of the surfaces.Samples threatened with MeOH allow cell adhesion and survival,promoting spreading,elongation and fusion of C2C12 muscle myoblast cells.A.Ronca F.Maiullari M.Milan V.Pace A.Gloria R.Rizzi R.De Santis L.Ambrosio 2017Bioactive Materials2017,2,3:1
2一种具有协同作用的新型除虫菊酯载热固体泡沫和苯甲酸苄酯对罪犯疥疮的疗效和耐受性的比较研究:ISAC研究(Studio Della scabbia in ambiente carcerario)Biele M. Campori G. Colombo R. M.Milan 罗素菊 2006世界核心医学期刊文摘(皮肤病学分册)2006,0,10:0
3Metabolomic studies in the inborn error of metabolism alkaptonuria reveal new biotransformations in tyrosine metabolism显示文摘Alkaptonuria (AKU) is an inherited disorder of tyrosine metabolism caused by lack of active enzyme homogentisate 1,2-dioxygenase (HGD). The primary consequence of HGD deficiency is increased circulating homogentisic acid (HGA), the main agent in the pathology of AKU disease. Here we report the first metabolomic analysis of AKU homozygous Hgd knockout (Hgd−/−) mice to model the wider metabolic effects of Hgd deletion and the implication for AKU in humans. Untargeted metabolic profiling was performed on urine from Hgd−/− AKU (n = 15) and Hgd+/− non-AKU control (n = 14) mice by liquid chromatography high-resolution time-of-flight mass spectrometry (Experiment 1). The metabolites showing alteration in Hgd−/− were further investigated in AKU mice (n = 18) and patients from the UK National AKU Centre (n = 25) at baseline and after treatment with the HGA-lowering agent nitisinone (Experiment 2). A metabolic flux experiment was carried out after administration of 13C-labelled HGA to Hgd−/−(n = 4) and Hgd+/−(n = 4) mice (Experiment 3) to confirm direct association with HGA. Hgd−/− mice showed the expected increase in HGA, together with unexpected alterations in tyrosine, purine and TCA-cycle pathways. Metabolites with the greatest abundance increases in Hgd−/− were HGA and previously unreported sulfate and glucuronide HGA conjugates, these were decreased in mice and patients on nitisinone and shown to be products from HGA by the 13C-labelled HGA tracer. Our findings reveal that increased HGA in AKU undergoes further metabolism by mainly phase II biotransformations. The data advance our understanding of overall tyrosine metabolism, demonstrating how specific metabolic conditions can elucidate hitherto undiscovered pathways in biochemistry and metabolism.Brendan P.Norman Andrew S.Davison Juliette H.Hughes Hazel Sutherland Peter J.M.Wilson Neil G.Berry Andrew T.Hughes Anna M.Milan Jonathan C.Jarvis Norman B.Roberts Lakshminarayan R.Ranganath George Bou-Gharios James A.Gallagher 2022Genes & Diseases2022,9,4:0
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