Institution
University of Aberdeen
Education•Aberdeen, United Kingdom•
About: University of Aberdeen is a education organization based out in Aberdeen, United Kingdom. It is known for research contribution in the topics: Population & Randomized controlled trial. The organization has 21174 authors who have published 49962 publications receiving 2105479 citations. The organization is also known as: Aberdeen University.
Papers published on a yearly basis
Papers
More filters
••
TL;DR: A meta-analysis of 104 functional neuroimaging studies using positron emission tomography/functional magnetic resonance imaging points to considerable functional segregation within rostral prefrontal cortex.
Abstract: One of the least well understood regions of the human brain is rostral prefrontal cortex, approximating Brodmann's area 10. Here, we investigate the possibility that there are functional subdivisions within this region by conducting a meta-analysis of 104 functional neuroimaging studies (using positron emission tomography/functional magnetic resonance imaging). Studies involving working memory and episodic memory retrieval were disproportionately associated with lateral activations, whereas studies involving mentalizing (i.e., attending to one's own emotions and mental states or those of other agents) were disproportionately associated with medial activations. Functional variation was also observed along a rostral-caudal axis, with studies involving mentalizing yielding relatively caudal activations and studies involving multiple-task coordination yielding relatively rostral activations. A classification algorithm was trained to predict the task, given the coordinates of each activation peak. Performance was well above chance levels (74% for the three most common tasks; 45% across all eight tasks investigated) and generalized to data not included in the training set. These results point to considerable functional segregation within rostral prefrontal cortex.
650 citations
••
TL;DR: A competing model that develops a non-resource-based account of self-control is advanced, suggesting that apparent regulatory failures reflect the motivated switching of task priorities as people strive to strike an optimal balance between engaging cognitive labor to pursue 'have- to' goals versus preferring cognitive leisure in the pursuit of 'want-to' goals.
648 citations
••
01 Feb 2015TL;DR: Predicting the impact of diet upon such a complex and interactive system as the human gut microbiota not only requires more information on the component groups involved but, increasingly, the integration of such information through modelling approaches.
Abstract: The gut microbiota and its metabolic products interact with the host in many different ways, influencing gut homoeostasis and health outcomes. The species composition of the gut microbiota has been shown to respond to dietary change, determined by competition for substrates and by tolerance of gut conditions. Meanwhile, the metabolic outputs of the microbiota, such as SCFA, are influenced both by the supply of dietary components and via diet-mediated changes in microbiota composition. There has been significant progress in identifying the phylogenetic distribution of pathways responsible for formation of particular metabolites among human colonic bacteria, based on combining cultural microbiology and sequence-based approaches. Formation of butyrate and propionate from hexose sugars, for example, can be ascribed to different bacterial groups, although propionate can be formed via alternative pathways from deoxy-sugars and from lactate by a few species. Lactate, which is produced by many gut bacteria in pure culture, can also be utilised by certain Firmicutes to form butyrate, and its consumption may be important for maintaining a stable community. Predicting the impact of diet upon such a complex and interactive system as the human gut microbiota not only requires more information on the component groups involved but, increasingly, the integration of such information through modelling approaches.
648 citations
••
TL;DR: Capecitabine is a novel fluoropyrimidine carbamate rationally designed to generate 5-fluorouracil preferentially in tumors, which is explained to a great extent by the activity of TP in colorectal tumor tissue, (the enzyme responsible for the conversion of 5′-DFUR to 5-FU), which is approximately four times that in adjacent healthy tissue.
Abstract: Purpose: Capecitabine (Xeloda) is a novel fluoropyrimidine carbamate rationally designed to generate 5-fluorouracil (5-FU) preferentially in tumors. The purpose of this study was to demonstrate the preferential activation of capecitabine, after oral administration, in tumor in colorectal cancer patients, by the comparison of 5-FU concentrations in tumor tissues, healthy tissues and plasma. Methods: Nineteen patients requiring surgical resection of primary tumor and/or liver metastases received 1,255 mg/m2 of capecitabine twice daily p.o. for 5–7 days prior to surgery. On the day of surgery, samples of tumor tissue, adjacent healthy tissue and blood samples were collected simultaneously from each patient, 2 to 12 h after the last dose of capecitabine had been administered. Concentrations of 5-FU in various tissues and plasma were determined by HPLC. The activities of the enzymes (CD, TP and DPD) involved in the formation and catabolism of 5-FU were measured in tissue homogenates, by catabolic assays. Results: The ratio of 5-FU concentrations in tumor to adjacent healthy tissue (T/H) was used as the primary marker for the preferential activation of capecitabine in tumor. In primary colorectal tumors, the concentration of 5-FU was on average 3.2 times higher than in adjacent healthy tissue (P=0.002). The mean liver metastasis/healthy tissue 5-FU concentration ratio was 1.4 (P=0.49, not statistically different). The mean tissue/plasma 5-FU concentration ratios exceeded 20 for colorectal tumor and ranged from 8 to 10 for other tissues. Conclusions: The results demonstrated the preferential activation of capecitabine to 5-FU in colorectal tumor, after oral administration to patients. This is explained to a great extent by the activity of TP in colorectal tumor tissue, (the enzyme responsible for the conversion of 5′-DFUR to 5-FU), which is approximately four times that in adjacent healthy tissue. In the liver, TP activity is approximately equal in metastatic and healthy tissue, which explains the lack of preferential activation of capecitabine in these tissues.
647 citations
••
TL;DR: The aim of this study was to review the definition and measurement of anastomotic leak after oesophagogastric, hepatopancreaticobiliary and lower gastrointestinal surgery.
Abstract: Background: Anastomotic leak after gastrointestinal surgery is an important postoperative event that leads to significant morbidity and mortality. Postoperative leak rates are frequently used as an indicator of the quality of surgical care provided. Comparison of rates between and within institutions depends on the use of standard definitions and methods of measurement of anastomotic leak. The aim of this study was to review the definition and measurement of anastomotic leak after oesophagogastric, hepatopancreaticobiliary and lower gastrointestinal surgery. Methods: A systematic review was undertaken of the published literature. Searches were carried out on five bibliographical databases (Medline, Embase, The Cochrane Library, Cumulative Index for Nursing and Allied Health Literature and HealthSTAR) for English language articles published between 1993 and 1999. Articles were critically appraised by two independent reviewers and data on definition and measurement of anastomotic leak were extracted. Results: Ninety-seven studies were reviewed and a total of 56 separate definitions of anastomotic leak were identified at three sites: upper gastrointestinal (13 definitions), hepatopancreaticobiliary (14) and lower gastrointestinal (29). The majority of studies used a combination of clinical features and radiological investigations to define and detect anastomotic leak. Conclusion: There is no universally accepted definition of anastomotic leak at any site. The definitions and values used to measure anastomotic failure vary extensively and preclude accurate comparison of rates between studies and institutions.
646 citations
Authors
Showing all 21424 results
Name | H-index | Papers | Citations |
---|---|---|---|
Paul M. Thompson | 183 | 2271 | 146736 |
Feng Zhang | 172 | 1278 | 181865 |
Ian J. Deary | 166 | 1795 | 114161 |
Peter A. R. Ade | 162 | 1387 | 138051 |
David W. Johnson | 160 | 2714 | 140778 |
Pete Smith | 156 | 2464 | 138819 |
Naveed Sattar | 155 | 1326 | 116368 |
John R. Hodges | 149 | 812 | 82709 |
Ruth J. F. Loos | 142 | 647 | 92485 |
Alan J. Silman | 141 | 708 | 92864 |
Michael J. Keating | 140 | 1169 | 76353 |
David Price | 138 | 1687 | 93535 |
John D. Scott | 135 | 625 | 83878 |
Aarno Palotie | 129 | 711 | 89975 |
Rajat Gupta | 126 | 1240 | 72881 |