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| 1 | The triterpenoid CDDO inhibits expression of matrix metalloproteinase-1,matrix metalloproteinase-13 and Bcl-3 in primary human chondrocytes显示文摘 | Elliott Sarah Hays Ezra | 2003 | Arthritis Research&Therapy2003，5，5： | 1 |
| 2 | The triterpenoid CDDO inhibits expression of matrix metalloproteinase-1,matrix metalloproteinase-13 and Bcl-3 in primary human chondrocytes显示文摘 | Sarah Elliott Ezra Hays Michael Mayor | 2003 | Arthritis Res Ther2003，5，5： | 1 |
| 3 | A pharmacist-led information technology intervention for medication errors (PINCER): a multicentre, cluster randomised, controlled trial and cost-effectiveness analysis显示文摘 | Anthony J Avery Sarah Rodgers Judith A Cantrill Sarah Armstrong Kathrin Cresswell Martin Eden Rachel A Elliott Rachel Howard Denise Kendrick Caroline J Morris Robin J Prescott Glen Swanwick Matthew Franklin Koen Putman Matthew Boyd Aziz Sheikh | 2012 | The Lancet . 2012 (9823)2012，，： | 1 |
| 4 | Biochemical analysis of the interactions of IQGAP1 C-terminal domain with CDC42显示文摘AIM:To understand the interaction of human IQGAP1 and CDC42,especially the effects of phosphorylation and a cancer-associated mutation. METHODS:Recombinant CDC42 and a novel C-termi- nal fragment of IQGAP1 were expressed in,and puri- fied from,Escherichia coli.Site directed mutagenesis was used to create coding sequences for three phos- phomimicking variants(S1441E,S1443D and S1441E/ S1443D)and to recapitulate a cancer-associated mu- tation(M1231I).These variant proteins were also ex- pressed and purified.Protein-protein crosslinking using 1-Ethyl-3-(3-dimethylaminopropyl)carbodiimide was used to investigate interactions between the C-terminal fragment and CDC42.These interactions were quanti- fied using surface plasmon resonance measurements.Molecular modelling was employed to make predictions about changes to the structure and flexibility of the protein which occur in the cancer-associated variant. RESULTS:The novel,C-terminal region of human IQGAP1 (residues 877-1558)is soluble following expression and purification.It is also capable of binding to CDC42,as judged by crosslinking experiments.Interaction appears to be strongest in the presence of added GTP.The three phosphomimicking mutants had different affini- ties for CDC42.S1441E had an approximately 200-fold reduction in affinity compared to wild type.This was caused largely by a dramatic reduction in the associa- tion rate constant.In contrast,both S1443D and the double variant S1441E/S1443D had similar affinities to the wild type.The cancer-associated variant,M1231I, also had a similar affinity to wild type.However,in the case of this variant,both the association and dis- sociation rate constants were reduced approximately 10-fold.Molecular modelling of the M1231I variant, based on the published crystal structure of part of the C-terminal region,revealed no gross structural changes compared to wild type(root mean square deviation of 0.564over 5556 equivalent atoms).However,pre- dictions of the flexibility of the polypeptide backbone suggested that some regions of the variant protein had greatly increased rigidity compared to wild type.One such region is a loop linking the proposed CDC42 bind- ing site with the helix containing the altered residue.It is suggested that this increase in rigidity is responsible for the observed changes in association and dissocia- tion rate constants. CONCLUSION:The consequences of introducing nega- tive charge at Ser-1441 or Ser-1443 in IQGAP1 are dif- ferent.The cancer-associated variant M1231I exerts its effects partly by rigidifying the protein. | Sarah F Elliott George Allen David J Timson | 2012 | World Journal of Biological Chemistry2012，3，3： | 1 |
| 5 | Making Effective Links to Decision-making:Key Challenges for Health Impact Assessment显示文摘 | Elliott Eva Francis Sarah | 2005 | Environmental Impact Assessment Review2005，25，： | 1 |
| 6 | An ecosystem-based approach to marine risk assessment显示文摘Risk assessments quantify the probability of undesirable events along with their consequences.They are used to prioritize management interventions and assess tradeoffs,serving as an essential component of ecosystem-based management(EBM).A central objective of most risk assessments for conservation and management is to characterize uncertainty and impacts associated with one or more pressures of interest.Risk assessments have been used in marine resource management to help evaluate the risk of environmental,ecological,and anthropogenic pressures on species or habitats including for data-poor fisheries management(e.g.,toxicity,probability of extinction,habitat alteration impacts).Traditionally,marine risk assessments focused on singular pressure-response relationships,but recent advancements have included use of risk assessments in an EBM context,providing a method for evaluating the cumulative impacts of multiple pressures on multiple ecosystem components.Here,we describe a conceptual framework for ecosystem risk assessment(ERA),highlighting its role in operationalizing EBM,with specific attention to ocean management considerations.This framework builds on the ecotoxicological and conservation literature on risk assessment and includes recent advances that focus on risks posed by fishing to marine ecosystems.We review how examples of ERAs from the United States fit into this framework,explore the variety of analytical approaches that have been used to conduct ERAs,and assess the challenges and data gaps that remain.This review discusses future prospects for ERAs as EBM decision-support tools,their expanded role in integrated ecosystem assessments,and the development of next-generation risk assessments for coupled natural-human systems. | Kirstin Holsman Jameal Samhouri Geoffrey Cook Elliott Hazen Erik Olsen Maria Dillard Stephen Kasperski Sarah Gaichas Christopher R.Kelble Mike Fogarty Kelly Andrews | 2017 | Ecosystem Health and Sustainability2017，3，1： | 0 |
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