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		题名	作者	年代	出处	被引量
	1	Cardiac resynchronization therapy can reverse abnormal myocardial strain distribution in patients with heart failure and left bundle branch block显示文摘	Ole-A Breithardt Christoph Stellbrink Lieven Herbots Piet Claus Anil M Sinha Bart Bijnens Peter Hanrath George R Sutherland	2003	Journal of the American College of Cardiology2003，，：	1
	2	Pelvic floor m uscle training after prostate surgery 显示文摘	Patricia Neumann Peter Sutherland Irmina Nahon	2012	Correspondence2012，379，：	1
	3	Relations of Plasma Matrix Metalloproteinase-9 to Clinical Cardiovascular Risk Factors and Echocardiographic Left Ventricular Measures: The Framingham Heart Study显示文摘	Johan Sundstr?m Jane C. Evans Emelia J. Benjamin Daniel Levy Martin G. Larson Douglas B. Sawyer Deborah A. Siwik Wilson S. Colucci Patrice Sutherland Peter W.F. Wilson Ramachandran S. Vasan	2004	Circulation: Journal of the American Heart Association2004，，23：	1
	4	Response of rat osteoblast-like cells to microstructured model surfaces in vitro显示文摘	Haihong Liao Ann-Sofie Andersson Duncan Sutherland Sarunas Petronis Bengt Kasemo Peter Thomsen	2002	Biomaterials2002，，4：	1
	5	NO-loaded Zn 2+ -exchanged zeolite materials: A potential bifunctional anti-bacterial strategy显示文摘	Sarah Fox Tom S. Wilkinson Paul S. Wheatley Bo Xiao Russell E. Morris Alistair Sutherland A. John Simpson Peter G. Barlow Anthony R. Butler Ian L. Megson Adriano G. Rossi	2009	Acta Biomaterialia2009，，4：	1
	6	A resource query interface for network-aware applications显示文摘	Bruce Lowekamp Nancy Miller Thomas Gross Peter Steenkiste Jaspal Subhlok Dean Sutherland	1999	Cluster Computing1999，，2：	1
	7	Association of Fibrinogen With Cardiovascular Risk Factors and Cardiovascular Disease in the Framingham Offspring Population显示文摘	James J. Stec Halit Silbershatz Geoffrey H. Tofler Travis H. Matheney Patrice Sutherland Izabela Lipinska Joseph M. Massaro Peter F. W. Wilson James E. Muller Ralph B. D’Agostino	2000	Circulation: Journal of the American Heart Association2000，，14：	1
	8	Cardiac resynchronization therapy can reverse abnormal myocardial strain distribution in patients with heart failure and left bundle branch block显示文摘	Ole-A Breithardt Christoph Stellbrink Lieven Herbots Piet Claus Anil M Sinha Bart Bijnens Peter Hanrath George R Sutherland	2003	Journal of the American College of Cardiology2003，，3：	1
	9	Applying CTs with Digital Ground Relays显示文摘	Peter E Sutherland	2001	IEEE Industry Applications Magazine2001，，：	1
	10	Innovative approaches towards an economic fusion reactor显示文摘Nuclear fusion potentially offers a clean;environmentally friendly and intrinsically safe energy source with an abundant fuel supply.Magnetic fusion energy research is approaching a new era of fusion power reactor design and construction planning.New physics understanding and powerful predictive tools have become available for improving fusion performance,developing and optimizing various magnetic confinement concepts.Emerging transformative enabling technologies can potentially mitigate and transform some present physics challenges from the possibly insurmountable to the potentially solvable.	Houyang Guo Francis Y C Thio Michl W Binderbauer Richard J Buttery Thomas R Jarboe Rajesh Maingi John S Sarff Peter C Stangeby Derek A Sutherland Mickey R Wade Michael C Zarnstorff	2020	National Science Review2020，7，2：	0
	11	Metabolomic 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	2022	Genes & Diseases2022，9，4：	0

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